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Coronoid hyperplasia: A review
Journal Pre-proof Coronoid Hyperplasia: A Review Yet Ching Goh Chuey Chuan Tan Daniel Lim Dr
PII:
S2468-7855(19)30305-2
DOI:
https://doi.org/doi:10.1016/j.jormas.2019.12.019
Reference:
JORMAS 789
To appear in:
Journal of Stomatology oral and Maxillofacial Surgery
Received Date:
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Accepted Date:
18 December 2019
Please cite this article as: Goh YC, Tan CC, Lim D, Coronoid Hyperplasia: A Review, Journal of Stomatology oral and Maxillofacial Surgery (2020), doi: https://doi.org/10.1016/j.jormas.2019.12.019
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CORONOID HYPERPLASIA: A REVIEW Yet Ching Goh Department of Oral and Maxillofacial Clinical Sciences, Faculty of Dentistry, University of Malaya, 50603 Kuala Lumpur, Malaysia Chuey Chuan Tan
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Department of Oral and Maxillofacial Clinical Sciences,
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Faculty of Dentistry, University of Malaya,
Daniel Lim
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50603 Kuala Lumpur, Malaysia
Faculty of Dentistry, University of Malaya,
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50603 Kuala Lumpur, Malaysia
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Department of Oral and Maxillofacial Clinical Sciences,
Corresponding author Dr Daniel Lim
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Department of Oral and Maxillofacial Clinical Sciences, Faculty of Dentistry, University of Malaya,
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50603 Kuala Lumpur, Malaysia.
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Tel No.: +603-79674807
Fax No.: +603-79674534
E-mail: [email protected] Disclosure of interest
The authors declare that they have no competing interest ABSTRACT Coronoid hyperplasia is one of the rare causes of progressive limitation of mouth opening due to impingement of the enlarged coronoid process of the mandible on the zygomatic bone. A
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review was performed on all cases reports and case series on coronoid hyperplasia. Gender, age at treatment, age of onset, types of hyperplasia (unilateral/bilateral), associated history, treatment, surgical approach, pre-operative mouth opening, intra-operative mouth opening, mouth opening at follow up and follow up period were recorded and analyzed. A total of 82 articles which reported 115 cases were included. Coronoid hyperplasia was commonly reported at mean age of 22.64 years
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old with male preponderance. Most of the cases were diagnosed and treated between the age of
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11-20 years old. This condition commonly involved bilateral coronoid process of mandible. The mean width of pre-operative mouth opening was 16.5mm and was improved to a mean mouth
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opening of 36.3mm intra operatively. Mean mouth opening was 34.8mm at an average follow up
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of 19 months. While the etiopathogenesis of coronoid hyperplasia is still not conclusive, treatment
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with either coronoidectomy or coronoidotomy produced good improvement in mouth opening. Keywords: mandible; coronoid process; hyperplasia; elongation; enlargement
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1. INTRODUCTION
The temporomandibular joint (TMJ) is a complex joint which provides articulation
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between the fixed temporal bone of the cranium and the movable mandible. The TMJs are bilateral,
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diarthrodial, lined by synovial membrane and freely movable joints [1]. Besides mandibular condyle, coronoid process is the other process that is attached to the ramus of mandible. This “crown-like” process of the mandible serves mainly as the attachment for temporalis muscle and partly for masseter muscle on its lateral surface. Aside from this, coronoid process does not have other role in the function of the jaw. Because of this, coronoid process can be removed either as a source of bone graft or as a result of pathology without posing any functional issues. This accessory process of the mandible can be either of triangular, rounded or hook shaped. Majority of the process are of triangular shape (49% - 67%), followed by hook shaped (21% - 30%) and the
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rounded process (3% - 24.58%) [2]. The length of coronoid process ranges from 13.9mm to 15.3mm with the right side longer than the left. The length is not affected by gender [3]. Coronoid process enlargement is relatively uncommon, and this condition leads to impingement of the coronoid process on the zygomatic bone restricting mandibular opening [4-6]. It can either be a true hyperplasic phenomenon or due to the presence of pathology lesions [4]. Coronoid process
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hyperplasia is an abnormal elongation of the mandibular coronoid process consisting of
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histologically normal bone [6]. Progressive reduction of mouth opening is the most consistent symptom [4,5]. The etiology of coronoid process hyperplasia is unclear to date, but several theories
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have been suggested [4,5]. This paper aims to provide a summary of reported cases of coronoid
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hyperplasia with regards to demographic details, etiopathology, clinical features and outcome from
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the treatments provided. 2. METHODS
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We performed this review with the intention to summarize findings from all the available literatures to provide an update on coronoid hyperplasia. PubMed and EBSCO database were used
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to search for relevant articles. In the search, the following keywords were used ‘coronoid’ and
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‘hyperplasia’. For the term ‘coronoid’, synonyms ‘coronoid process’ was entered. For term ‘hyperplasia’, synonyms ‘enlargement’ and ‘elongation’ were entered. Boolean operator OR was applied between synonyms and operator AND was used between the two search terms. This review included all case reports and case series in English language found in PubMed and EBSCO using the search terms. No limit was imposed on the publication year. Assessment of the titles and abstracts were carried out to select relevant articles. Reference lists of the selected articles were checked to trace additional articles that are not found in both PubMed and EBSCO.
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Full texts of the relevant articles were then retrieved either through online databases or hand search. Cases with histopathology and/or morphology of osteochondroma were excluded. Data extracted from the included articles were gender, age at treatment, age of onset, types of hyperplasia (unilateral/bilateral), associated history, treatment, surgical approach, pre-operative mouth opening, intra-operative mouth opening, mouth opening at follow up and duration of follow
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up. Descriptive analysis was employed. Data analysis were completed using SPSS version 24. 3. RESULTS
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Literature search was performed on the 15th July 2019. A total of 742 articles were obtained
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from both PubMed and EBSCO. After removing duplicates, non-relevant articles and osteochondroma cases, a total of 82 articles reporting 115 cases were included in this review (Table
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1).
The mean reported age at diagnosis was 22.64 years old. The youngest patient reported
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was 0.25 years old while the oldest patient was 66 years old. Majority (42.6%, n=49) of the patients
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were in the age group of 11 to 20 years old followed by age group of 21 to 30 years old (26.1%, n=30). On the other hand, the mean onset age was 14.7 years old. Similar to the age at diagnosis,
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majority of the patients’ age of onset was between 11 to 20 years old. However, as many as 52 articles failed to provide history of onset of the disease. From this review, it is evident that coronoid hyperplasia was of male preponderance, with male to female ratio of 5:1. Hyperplasia of both coronoid processes were the most reported, representing 79.1% of the reported cases, while the rest were unilateral cases. While most of the cases were idiopathic (66.1%, n=76), considerable amount of cases (9.6%, n=11) were attributed to previous history of trauma. Other less common histories were temporomandibular joint disorders, Moebius Syndrome, mild torticollis, nevoid
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basal cell carcinoma of skin, pseudocamptodactyly, ear infection and even difficult dental extraction. Progressive reduction of mouth opening is the hallmark of coronoid hyperplasia. The range of mouth opening in patients affected by coronoid hyperplasia was between 2mm-38mm. Generally, the mean pre-operative mouth opening was 16.5mm. However, it is worth mentioning
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that pre-operative mouth opening was not reported in 4 cases. On the other hand, intra-operative
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mouth opening averaged at 36.3mm with the range of 10mm-60mm. Almost half (45.2%, n=52)
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of the literature did not report their intra-operative achievements. As there is no proper follow-up guideline available, the range of follow-up period differed from as short as 1 month to the longest
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144 months. The mean follow-up period was around 19 months. Follow-up protocol was not
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mentioned in 44 cases. In 73 cases, the authors recorded the final width of mouth opening at the end of their follow-up. This width ranged from as low as 2mm to as high as 65mm. The mean final mouth opening was 34.8mm, which was almost the same as the mouth opening achieved during
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surgery. Apart from limited mouth opening, facial asymmetry and temporomandibular joint
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disorders were other more commonly reported signs and symptoms.
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There are mainly two types of surgical treatment provided. Coronoidectomy was performed in 76.5% (n=88) of the cases while coronoidotomy was performed in 8.7% (n=10) of the cases. No surgery was performed in 14 cases either due to age factor or patients were not keen for treatment. However, details of treatment provided were not mentioned in 3 cases. Intraoral approach was the preferred approach as it was used in 61.7% (n=71) of the cases. Extraoral approach was only used in a small number of patients (13%, n=15). To gain better access, surgeons performed surgery via both intraoral and extraoral approaches in 6 patients. Only one group of authors reported the use of endoscope via intraoral approach while performing coronoidectomy.
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4. DISCUSSION Till date, pathogenesis of coronoid hyperplasia remains unknown. As a result, various hypotheses had been put forward to explain the pathogenesis. As with most other diseases, role of genes in the pathogenesis was coined by various authors following cases that were encountered. van Hoof and Besling observed bilateral coronoid hyperplasia in patients with trismus-
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pseudocamptodactyly syndrome [80]. This syndrome is inherited in an autosomal dominant
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fashion. Hecht and Beals also reported similar presentation in their patients [88]. Veugelers et al
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did a sequence analysis on large kindred affected by trismus-pseudocamptodactyly syndrome and found a mutation of MYH8 gene. This gene encodes for class II myosin heavy chains which is
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important for skeletal muscle contraction [89]. In 2002, Leonardi et al reported the occurrence of
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coronoid hyperplasia in patients with nevoid basal cell carcinoma syndrome which may suggest possible genetic role in development of coronoid hyperplasia [90]. Apart from association with other diseases, coronoid hyperplasia was also reported in a pair of identical twins. This report
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further convinces the genetic basis hypotheses [5]. This review shows most of the cases involved
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both sides of coronoid process. This reflects a possible systemic effect governs by genetic factors
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rather than local factors. However, more studies are needed to prove this association. Role of hormone had also been associated with coronoid hyperplasia. This was coined by Rowe in 1963 as he observed this condition in two of his patients who presented to him at the age of 15 [87]. However, the role of hormone was not favored due to lack of evidence. Echoing Rowe’s idea, in this review, we observed that most of the patients presented between the age of 11-20 years old coinciding with the normal growth spurt. Thus, we felt that further studies on hormonal role in coronoid hyperplasia are necessary.
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Coronoid hyperplasia was also thought to be associated with temporomandibular disorders. It is commonly seen together with untreated temporomandibular joint ankylosis. In this condition, there is complex muscular interactions between the elevator and depressor muscles of the jaw trying to maintain normal jaw function. As a result of this, temporalis muscle undergoes hyperemia, atrophy and eventually fibrosis. Due to its myostatic contracture state, fibrosed tendon
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of temporalis muscle causes hyperactivity of the suprahyoid muscles during mouth opening. In
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turn, the suprahyoid muscles induce isometric contraction of temporalis muscle due to the function of mandibular reciprocal inhibition [91,92]. Ultimately, hyperplasia or elongation of the coronoid
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process occurs under the contraction force of temporalis muscle akin to distraction osteogenesis
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[93]. While Farrar and McCarty suggested that coronoid hyperplasia maybe related to existing temporomandibular joint disorders [94], Isberg et al specifically linked it with prolonged
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temporomandibular joint disc displacement [95]. It is important to note that both coronoid hyperplasia and chronic TMJ disc displacement produce almost similar clinical presentation which
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are progressive limitation of mouth opening with ipsilateral jaw deviation, in unilateral cases. This
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renders initial diagnosis challenging, especially borderline cases, without radiographic investigations. It was observed that some cases were initially diagnosed with TMJ disorders
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following patients’ clinical presentations; but were later diagnosed as coronoid hyperplasia following radiographic findings. Their signs and symptoms were relieved following treatment of the hyperplastic coronoid process. In connection with TMJ disorders, Wenghoefer et al in 2008 reported coronoid hyperplasia in patients with ankylosing spondylitis. Although they believed that TMJ can be affected similar to the sacroiliac joint, but they were unable to prove this under the microscope [96].
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Some authors attributed coronoid hyperplasia to previous facial trauma. Trauma to the zygoma [23,30] and mandible [21,41] had been reported so far. It was postulated that following facial trauma, tensile forces of the temporalis muscle exerted on the coronoid process was akin to distraction osteogenesis leading to elongation of the process [23]. On the other hand, Smyth and Wake were of the opinion that coronoid process hyperplasia occurred following torn temporalis
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tendon near its insertion which lead to hematoma formation and subsequent clot organization
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leading to new bone forming at the coronoid [50].
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The role of temporalis muscle activity cannot be disregarded in the pathogenesis of coronoid hyperplasia as it is the main structure that attaches to the coronoid process. Sarnat and
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Engel back in 1951, proposed that hyperactivity of temporalis muscle could be the cause of
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coronoid hyperplasia [97]. Jamal et al reported that contralateral coronoid process showed elongation following hemimandibulectomy with disarticulation [98]. In these cases, loss of half of the mandible possibly led to increased muscular activity of the contralateral temporalis as the jaw
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elevator. Prolonged increased muscular pull on the coronoid might lead to its elongation. Puche et
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al hypothesized the role of congenital hypotonia in the development of coronoid hyperplasia. They
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believed that reduced mandibular movements and deglutition could have led to relative hyperactivity of temporalis muscle which was not counterbalanced by infra and suprahyoid muscles may be the cause of coronoid hyperplasia in two of their patients [99]. However, Gerbino et al and Hall et al refuted the role of hyperactive temporalis muscle. Their rebuttals were supported by normal electromyography findings in their patients with hyperplastic coronoid [5,56]. Although none of the hypotheses mentioned have strong evidence to support them, we can notice that most of these hypotheses suggested a crucial role of temporalis muscle in the pathogenesis of coronoid hyperplasia either directly or indirectly.
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In most of the operated cases, coronoidectomy was the treatment of choice. This procedure involves removal of the osteotomized coronoid process. Prior to completion of the osteotomy, some authors tied a stainless-steel wire to the coronoid process through a hole made using round bur or to a screw anchored to the coronoid process while others held it with forceps [12,53]. This was to avoid the osteotomized coronoid process from being pulled superiorly by temporalis muscle
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rendering subsequent removal more challenging. A few authors performed coronoidotomy by
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leaving the coronoid segment in-situ following osteotomy. Advocators of this techniques reported good outcome as the hyperplastic coronoid process had been separated from the rest of the
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mandible making its movements unhindered by the zygomatic bone [5,31]. Besides that,
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coronoidotomy also requires less tissue reflection therefore reducing tissue damage and scarring. Despite simplicity of this technique, it comes with the risk of coronoid process reunion with the
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ramus [31]. To overcome this risk, Chen et al performed modified (gap) coronoidotomy which involved removal of a strip of bone from the base of coronoid process thus creating a gap of 5-
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6mm between coronoid process and ramus [100]. Mulder and his colleagues summarized in their
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review that coronoidotomy had better post-operative results, although not significant, compared to coronoidectomy despite the latter being treatment of choice [6]. Access to the coronoid process
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can be achieved either via intraoral or extraoral approaches. The choice of approach depends on the amount of mouth opening and surgeon’s experience. Extraoral approach is preferred if the limitation of mouth opening is severe. Among the extraoral approaches used were submandibular, pre-auricular and coronal approaches. Exposure of coronoid process is hindered by severe limitation of mouth opening. By using extraoral approach, complete coronoidectomy and myotomy, fasciotomy and zygomatic osteotomy can be performed. However, intraoral approach was more preferred due to the possible risk of facial nerve injury and external scar with extraoral
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approach. In an intraoral approach, incision is made along the external oblique ridge followed by stripping of temporalis muscle fibers from coronoid process prior to osteotomy. Robiony et al performed endoscopically assisted coronoidectomy in their patients and claimed the technique had less morbidity, faster and allow physical therapy to be started sooner [24]. Regardless of the types of treatment provided, post-operative physiotherapy plays a very
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important role in at least maintaining, if not improving, the width of mouth opening achieved
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during the surgery. Physiotherapy can be performed using spatulas, mouth screw, dynamic
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devices, wedge or Therabite® device. Although there was no study to compare which device is more superior for physiotherapy in coronoid hyperplasia, some authors advocated the use of
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Therabite® device as it is easy to use [34]. Its horseshoe-shaped surfaces are in contact with
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multiple anterior and posterior teeth, making it more comfortable and less stress on anterior teeth compared to spatulas and mouth screw. Spatulas and mouth screws are usually wedged between the upper and lower anterior teeth. Many authors advocated that aggressive physiotherapy must be
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performed during the first year of surgery.
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Dental panoramic tomography (DPT) was the most commonly used imaging modality to
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assist in the diagnosis of coronoid hyperplasia. Instead of using an absolute normal value of coronoid length as reference, Kubota et al in 1999 utilized Levandoski panographic analysis to aid in diagnosis of coronoid hyperplasia. They measured coronoid-gonion and condyle-gonion distances based on dental panoramic tomogram. Ratio of coronoid-gonion to condyle-gonion was later computed and they concluded a mean ratio of 0.94 was considered normal as opposed to 1.17 in diseased group. They suggested that patients with limited mouth opening and coronoidgonion:condyle-gonion ratio above 1.1 are likely to have coronoid hyperplasia [101]. However, it should be highlighted that these values were derived from a small group of 3 subjects with coronoid
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hyperplasia. With the availability of computed tomography, not only the hyperplastic coronoid process can be visualized but also its shape and its actual relation between coronoid process and the zygoma. Stopa and his colleagues later in 2013 measured the similar distances but based on 3D reconstruction of computed tomography scan. A ratio of up to 1.07 was considered as normal while ratio above 1.15 signified possibility of coronoid hyperplasia [102]. By using these methods
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of measurement, condition of the condyle has a great impact on the ratio. Any abnormalities in
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condylar length will give a false impression on the coronoid process.
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5. CONCLUSION
From this review, it can be observed that coronoid hyperplasia was mainly seen in the
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second decade of life and predominantly in male. It was commonly presented as bilateral cases.
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Despite the controversial etiologies, this condition can be treated with either coronoidectomy or coronoidotomy producing satisfactory outcome. However, it must be highlighted that the above
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inferences are made based on data available in the literatures included.
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REFERENCES
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[1] David CM, Elavarasi P. Functional anatomy and biomechanics of temporomandibular joint and the far-reaching effects of its disorders. J Adv Clin Res Insights 2016;3:101-106 [2] Tapas S. Morphological variations of coronoid process in dry adult human mandibles. Indian Journal of Basic and Applied Medical Research 2014;3(2):401-405 [3] Nayak S, Patra S, Singh G, Mohapatra C, Rath S. Study of the size of the coronoid process of mandible. IOSR Journal of Dental and Medical Sciences 2015;14(6):66-69
Page 11 of 36
[4] McLoughlin PM, Hopper C, Bowley NB. Hyperplasia of the mandibular coronoid process: An analysis of 31 cases and a review of literature. J Oral Maxillofac Surg 1995;53:250255 [5] Gerbino G, Bianchi SD, Bernardi M, Berrone S. Hyperplasia of the mandibular coronoid process: long-term follow-up after coronoidotomy. J Craniomaxillofac Surg 1997;25:169-
f
173
oo
[6] Mulder CH, Kalaykova SI, Gortzak RA Th. Coronoid process hyperplasia: a systematic review of the literature from 1995. Int J Oral Maxillofac Surg. 2012;41:1483-1489
pr
[7] Schneble EJ, Moore RD, Pettersson DR, Pollock JM, Barajas RF, Jr. Coronoid Process
e-
Hyperplasia : A Rare Disorder Masquerading as Temporomandibular Joint Disease. Clin Neuroradiol. 2019
Pr
[8] Tolentino MCA, Assis JS, Cardoso CAeA, Manzi FR. Mandibular coronoid process hyperplasia: a case report. Rev CEFAC 2018;20(3):400-405
al
[9] Ghazizadeh M, Sheikhi M, Salehi MM, Khaleghi A. Bilateral coronoid hyperplasia causing
[10]
rn
painless limitation of mandibular movement. Radiol Case Rep. 2018;13(1):112-117 Ribeiro da Silva J, Pereira RDS, Agueda C, Nunes PM, Marin C, Hochuli-Vieira
Jo u
E. Bilateral Coronoid Hyperplasia in a 43-Year-Old Patient Treated With Intraoral Coronoidectomy. J Craniofac Surg. 2017;28(4):e402-e403 [11]
Starch-Jensen T, Kjellerup AD. Bilateral Elongated Mandibular Coronoid Process
and Restricted Mouth Opening: A Case Report. Open Dent J. 2017;11:670-678 [12]
Romano M, Porcellini G, Rossi D, Bolzoni A, Gianni AB, Silvestre FJ, et al.
Bilateral coronoid hyperplasia: a report of six cases. J Biol Regul Homeost Agents. 2017;31(2 Suppl 1):139-145
Page 12 of 36
[13]
Acharya P, Stewart A, Naini FB. Coronoid impingement syndrome: literature
review and clinical management. Maxillofac Plast Reconstr Surg. 2017;39(1):11 [14]
Silky R Punyani VRJ. Unilateral acquired condylar hypoplasia and coronoid
hyperplasia of the mandible. 2017;10:198-201 [15]
Khandavilli SD, Pattni N, Naredla PR, Williams R. First case of bilateral coronoid
f
hyperplasia in monozygotic twin sisters-a new aetiological perspective? Oral Maxillofac
[16]
oo
Surg. 2016;20(4):441-443
Monevska DP, Benedetti A, Popovski V, Naumovski S, Grcev A, Bozovic S, et al.
pr
Mandibular Movement Restoration in a Child with Bilateral Coronoid Hyperplasia: A Case
[17]
e-
Report. Open Access Maced J Med Sci. 2016;4(2):293-295
Balkin DM, Chen I, Oberoi S, Pomerantz JH. Bilateral Coronoidectomy by
2015;26(6):1954-1956
Choi MG, Kim DH, Ki EJ, Cheon HM. Trismus Due to Bilateral Coronoid
al
[18]
Pr
Craniofacial Approach for Hecht Syndrome-Related Trismus. J Craniofac Surg.
[19]
rn
Hyperplasia. Maxillofac Plast Reconstr Surg. 2014;36(4):168-172 Kim SM, Lee JH, Kim HJ, Huh JK. Mouth opening limitation caused by coronoid
Jo u
hyperplasia: a report of four cases. J Korean Assoc Oral Maxillofac Surg. 2014;40(6):301307 [20]
Utsman RA, Klasser GD, Padilla M. Coronoid hyperplasia in a pediatric patient:
case report and review of the literature. J Calif Dent Assoc. 2013;41(10):766-770 [21]
Sleeman D, Warren E, McAuliffe M. Unilateral coronoid hyperplasia associated
with early childhood facial trauma: a case presentation. J Ir Dent Assoc. 2012;58(4):212214
Page 13 of 36
[22]
Newaskar V, Idrees F, Patel P. Unilateral coronoid hyperplasia treated by
coronoidectomy using a transzygomatic approach. Natl J Maxillofac Surg. 2012;3(2):195198 [23]
Bayar GR, Akcam T, Gulses A, Sencimen M, Gunhan O. An excessive coronoid
hyperplasia with suspected traumatic etiology resulting in mandibular hypomobility.
Robiony M, Casadei M, Costa F. Minimally invasive surgery for coronoid
oo
[24]
f
Cranio. 2012;30(2):144-149
hyperplasia: endoscopically assisted intraoral coronoidectomy. J Craniofac Surg.
Costa YM, Porporatti AL, Stuginski-Barbosa J, Cassano DS, Bonjardim LR, Conti
e-
[25]
pr
2012;23(6):1838-1840
Dent J. 2012;23(3):252-255 [26]
Pr
PC. Coronoid process hyperplasia: an unusual cause of mandibular hypomobility. Braz
Ramalho-Ferreira G, Faverani LP, Fabris AL, Pastori CM, Magro-Filho O, Ponzoni
al
D, et al. Mandibular movement restoration through bilateral coronoidectomy by intraoral
[27]
rn
approach. J Craniofac Surg. 2011;22(3):988-991 Peacock ZS, Resnick CM, Faquin WC, Kaban LB. Accessory mandibular condyle
Jo u
at the coronoid process. J Craniofac Surg. 2011;22(6):2168-2171 [28]
Galie M, Consorti G, Tieghi R, Denes SA, Fainardi E, Schmid JL, et al. Early
surgical treatment in unilateral coronoid hyperplasia and facial asymmetry. J Craniofac Surg. 2010;21(1):129-133 [29]
Vaidhyanath R, Raj V. Mandibular coronoid process hyperplasia causing restricted
mouth opening. Br J Hosp Med (Lond). 2010;71(4):229
Page 14 of 36
[30]
Iqbal S, Hamid ALA, Purmal K. Unilateral coronoid hyperplasia following trauma:
a case report. Dental Traumatology. 2009;25(6):626-630 [31]
Yura S, Ohga N, Ooi K, Izumiyama Y. Mandibular coronoid hyperplasia: a case
report. Cranio. 2009;27(4):275-279 [32]
Zhong SC, Xu ZJ, Zhang ZG, Zheng YH, Li TX, Su K. Bilateral coronoid
f
hyperplasia (Jacob disease on right and elongation on left): report of a case and literature
[33]
oo
review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2009;107(3):e64-e67 Fernandez Ferro M, Fernandez Sanroman J, Sandoval Gutierrez J, Costas Lopez A,
pr
Lopez de Sanchez A, Etayo Perez A. Treatment of bilateral hyperplasia of the coronoid
e-
process of the mandible. Presentation of a case and review of the literature. Med Oral Patol Oral Cir Bucal. 2008;13(9):E595-E598
Gibbons AJ, Abulhoul S. Use of a Therabite appliance in the management of
Pr
[34]
bilateral mandibular coronoid hyperplasia. Br J Oral Maxillofac Surg. 2007;45(6):505-506 Mazzetto MO, Hotta TH. Hypertrophy of the mandibular coronoid process and
al
[35]
rn
structural alterations of the condyles associated with limited buccal opening: case report. Braz Dent J. 2007;18(2):171-174 Leovic D, Djanic D, Zubcic V. Mandibular locking due to bilateral coronoid
Jo u
[36]
process hyperplasia. Wien Klin Wochenschr. 2006;118(19-20):594 [37]
Kursoglu P, Capa N. Elongated mandibular coronoid process as a cause of
mandibular hypomobility. Cranio. 2006;24(3):213-216 [38]
Satoh K, Ohno S, Aizawa T, Imamura M, Mizutani H. Bilateral coronoid
hyperplasia in an adolescent: report of a case and review of the literature. J Oral Maxillofac Surg. 2006;64(2):334-338
Page 15 of 36
[39]
Bertacci A, Landi N, Manfredini D, Ferronato G, Bosco M. Coronoid hyperplasia.
A case report. Minerva Stomatol. 2005;54(7-8):461-470 [40]
Mano T, Ueyama Y, Koyama T, Nishiyama A, Matsumura T. Trismus due to
bilateral coronoid hyperplasia in a child: case report. J Oral Maxillofac Surg. 2005;63(3):399-401 Tieghi R, Galie M, Piersanti L, Clauser L. Bilateral hyperplasia of the coronoid
f
[41]
[42]
oo
processes: clinical report. J Craniofac Surg. 2005;16(4):723-726
Fabie L, Boutault F, Gas C, Paoli JR. Neonatal bilateral idiopathic hyperplasia of
Colquhoun A, Cathro I, Kumara R, Ferguson MM, Doyle TC. Bilateral coronoid
e-
[43]
pr
the coronoid processes: case report. J Oral Maxillofac Surg. 2002;60(4):459-462
hyperplasia in two brothers. Dentomaxillofac Radiol. 2002;31(2):142-146 Gibbons AJ, Byrne AJ, Key SJ. Trismus due to bilateral mandibular coronoid
Pr
[44]
hyperplasia. J R Army Med Corps. 2001;147(3):311-313 Leonardi R, Sorge G, Caltabino M. Bilateral hyperplasia of the mandibular
al
[45]
rn
coronoid processes associated with the nevoid basal cell carcinoma syndrome in an Italian boy. Br Dent J. 2001;190(7):349-350 Turk AE, McCarthy JG, Nichter LS, Thorne CH. Moebius syndrome: the new
Jo u
[46]
finding of hypertrophy of the coronoid process. J Craniofac Surg. 1999;10(1):93-96 [47]
Loh HS, Ling SY, Lian CB, Shanmuhasuntharam P. Bilateral coronoid hyperplasia-
-a report with a view on its management. J Oral Rehabil. 1997;24(10):782-787 [48]
Currie WJ, Stassen LF, Thompson WD. An unusual cause of trismus. Dent Update.
1995;22(2):72-73
Page 16 of 36
[49]
Gibbons AJ. Case report: Computed tomography in the investigation of bilateral
mandibular coronoid hyperplasia. Br J Radiol 1995;68:531-533 [50]
Smyth AG, Wake MJ. Recurrent bilateral coronoid hyperplasia: an unusual case.
Br J Oral Maxillofac Surg. 1994;32(2):100-104 [51]
Honig JF, Merten HA, Korth OE, Halling F. Coronoid process enlargement.
Fukumori T, Tagawa T, Inui M. Bilateral coronoid process hyperplasia and short
oo
[52]
f
Dentomaxillofac Radiol. 1994;23(2):108-110
stature. A case report. Int J Oral Maxillofac Surg. 1993;22(3):139-144 Totsuka Y, Fukuda H. Bilateral coronoid hyperplasia. Report of two cases and
pr
[53]
[54]
e-
review of the literature. J Craniomaxillofac Surg. 1991;19(4):172-177 Hayter JP, Robertson JM. Surgical access to bilateral coronoid hyperplasia using
[55]
Pr
the bicoronal flap. Br J Oral Maxillofac Surg. 1989;27(6):487-493 Shultz RE, Theisen FC. Bilateral coronoid hyperplasia. Report of a case. Oral Surg
Hall RE, Orbach S, Landesberg R. Bilateral hyperplasia of the mandibular coronoid
rn
[56]
al
Oral Med Oral Pathol. 1989;68(1):23-26
processes: a report of two cases. Oral Surg Oral Med Oral Pathol. 1989;67(2):141-145 Macleod AW. Limitation of mandibular opening due to enlarged coronoid
Jo u
[57]
processes. Aust Dent J. 1987;32(2):120-125 [58]
Giacomuzzi D. Bilateral enlargement of the mandibular coronoid processes: review
of the literature and report of case. J Oral Maxillofac Surg. 1986;44(9):728-731 [59]
Bronstein SL, Osborne JJ. Mandibular limitation due to bilateral coronoid
enlargement: management by surgery and physical therapy. Cranio. 1985;3(1):58-62
Page 17 of 36
[60]
Balcunas BA, Gallimore R. Bilateral coronoid hyperplasia. Dentomaxillofac
Radiol. 1985;14(1):41-44 [61]
Kreutz RW, Sanders B. Bilateral coronoid hyperplasia resulting in severe limitation
of mandibular movement. Report of a case. Oral Surg Oral Med Oral Pathol. 1985;60(5):482-484 Kraut RA. Bilateral coronoid hyperplasia: report of two cases. J Oral Maxillofac
f
[62]
[63]
oo
Surg. 1985;43(8):612-614
Praal FR. Limitation of mandibular movement due to bilateral mandibular coronoid
Tucker MR, Guilford WB, Howard CW. Coronoid process hyperplasia causing
e-
[64]
pr
process enlargement. J Oral Maxillofac Surg. 1984;42(8):534-536
restricted opening and facial asymmetry. Oral Surg Oral Med Oral Pathol. 1984;58(2):130-
[65]
Pr
132
Bernstein L, Fernandez B. Bilateral hyperplasia of the coronoid process of the
York BV, Cockerham S. Bilateral hyperplasia of the coronoid processes in siblings.
rn
[66]
al
mandible. Report of a case. Arch Otolaryngol. 1984;110(7):480-482
Oral Surg Oral Med Oral Pathol. 1983;56(6):584-585 Marra LM. Bilateral coronoid hyperplasia, a developmental defect. Oral Surg Oral
Jo u
[67]
Med Oral Pathol. 1983;55(1):10-13 [68]
Lucaya J, Herrera M, Vera J. Unilateral hyperplasia of the coronoid process in a
child: a cause of restricted opening of the mouth. Radiology. 1982;144(3):528 [69]
Javid B. Unilateral hyperplasia of the coronoid process of the mandible. Case
report. Int J Oral Surg. 1981;10(2):145-147
Page 18 of 36
[70]
Duffy BL. Case report--bilateral mandibular coronoid process hyperplasia. Anaesth
Intensive Care. 1980;8(4):484-486 [71]
Hecker R, Corwin JO. Bilateral coronoid hyperplasia: review of the literature and
report of case. J Oral Surg. 1980;38(8):606-608 [72]
Shuken RA, Girard KR. Bilateral mandibular coronoid hyperplasia. J Oral Surg.
Rivas PH. Reduction of mouth opening due to mandibular coronoid progess
oo
[73]
f
1979;37(10):744-746
enlargement. Report of a case. Oral Surg Oral Med Oral Pathol. 1979;47(2):131-134 Monks FT. Bilateral hyperplasia of the mandibular coronoid processes: a case
[75]
e-
report. Br J Oral Surg. 1978;16(1):31-37
pr
[74]
Michel RG, Hudson WR, Drawbaugh EJ, Baylin GJ. Exostosis of the mandibular
[76]
Pr
coronoid process. Ann Otol Rhinol Laryngol. 1977;86:12-16 Kallioniemi H, Oksala E, Lauttamus A. Unilateral hyperplasia of the mandibular
Shurman J. Bilateral hypertrophy of the coronoid processes. Anesthesiology.
rn
[77]
al
coronoid process. Case report. Proc Finn Dent Soc. 1975;71(5):184-190
1975;42(4):491-492
Scott AS, Frew AL, Jr. Bilateral enlargement of the mandibular coronoid processes
Jo u
[78]
in a patient with rheumatoid arthritis of the temporomandibular joints. J Oral Surg. 1975;33(10):787-789 [79]
Rusconi L, Brusati R. Restricted opening of the mouth from symmetrical bilateral
hyperplasia of the coronoid processes. J Oral Surg. 1974;32(6):452-456 [80]
van Hoof RF, Besling WFJ. Coronoid process enlargement. Br J Oral Surg
1973;10:339-348
Page 19 of 36
[81]
Bramley PA, Norman JE. Secondary enlargement of the mandibular coronoid
process. Br J Surg. 1972;59(6):426-429 [82]
Muldoon CJ. Bilateral coronoid hyperplasia. J Ir Dent Assoc. 1971;17(4):121-124
[83]
Hurd GK. Diagnosis and surgical management of coronoid process hyperplasia:
report of case. J Can Dent Assoc (Tor). 1970;36(10):373-375 Fitzpatrick BN. Bilateral hyperplasia of the mandibular coronoid process. Oral Surg
f
[84]
[85]
Nickerson JW, Jr., Grafft NL, Sazima HJ. Bilateral coronoid process enlargement:
pr
report of case. J Oral Surg. 1969;27(11):885-890
Allison ML, Wallace WR, Von Wyl H. Coronoid abnormalities causing limitation
e-
[86]
oo
Oral Med Oral Pathol. 1970;29(2):184-190
of mandibular movement. J Oral Surg. 1969;27(3):229-233
Pr
[87]Rowe NL. Bilateral Developmental Hyperplasia of the Mandibular Coronoid Process. A
Report of Two Cases. Br J Oral Surg. 1963;1:90-104 Hecht F, Beals. Inability to open mouth fully: an autosomal dominant phenotype
al
[88]
[89]
rn
with facultative campylodactyly and short stature. Birth Defects 1969;5:69-98 Veugelers M, Bressan M, McDermott DA et al. Mutation of perinatal myosin heavy
Jo u
chain associated with a Carney complex variant. N Eng J Med 2004;351:460-469 [90]
Leonardi R, Caltabiano M, Lo Muzio L, Gorlin RJ, Bucci P, Pannone G, Canfora
M, Sorge G. Bilateral hyperplasia of the mandibular coronoid process in patients with nevoid basal cell carcinoma syndrome: an undescribed sign. Am J Med Genet 2002; 110(4):400-403
Page 20 of 36
[91]
Mioche L, Bourdiol P, Martin JF, Noel Y. Variations in human masseter and
temporalis muscle activity related to food texture during free and side-imposed mastication. Arch Oral Biol 199;44:1005-1012 [92]
Armijo-Olivo S, Magee DJ. Electromyographic activity of the masticatory and
cervical muscles during resisted jaw opening movement. J Oral Rehabil 2007;34:184-194 Chakranarayan A, Jeyaraj P. Coronoid hyperplasia in chronic progressive trismus.
f
[93]
[94]
oo
Med Hypotheses 2011;77:863-868
Farrar WB, McCarty WL Jr. Inferior joint space arthrography and characteristics
Isberg A, Isacsson G, Nah KS. Mandibular coronoid process locking: a prospective
e-
[95]
pr
of condylar paths in internal derangements of the TMJ. J Prosthet Dent 1979;41:548-555
study of frequency and association with internal derangement of the temporomandibular
[96]
Pr
joint. Oral Surg Oral Med Oral Pathol 1987;63:275-279 Wenghoefer M, Martini M, Allam JP, Novak N, Reich R, Berge SJ. Hyperplasia of
al
the coronoid process in patients with ankylosing spondylitis (Bechterew disease). J
[97]
rn
Craniofac Surg 2008;19:1114-1118
Sarnat BG, Engel MB. A serial study of mandibular growth after removal of the
Jo u
condyle in the Macaca rhesus monkey. Plast Reconstr Surg 1951;7:364-380 [98]
Jamal BT, Taub D, Gold L. Contralateral coronoid hyperplasia in patients
undergoing hemimandibulectomy with disarticulation: a case series. J Oral Maxillofac Surg 2009;67(9):1821-1825 [99]
Puche M, Guijarro-Martínez R, Pérez-Herrezuelo G, Miragall L, Iglesias ME,
Martínez-Costa C. The hypothetical role of congenital hypotonia in the development of early coronoid hyperplasia. J Craniomaxillofac Surg 2012;40:e155-e158
Page 21 of 36
[100]
Chen CM, Chen CM, Ho CM, Huang IY. Gap coronoidotomy for management of
coronoid process hyperplasia of the mandible. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;112:e1-e4 [101]
Kubota Y, Takenoshita Y, Takamori K, Kanamoto M, Shirasuna K. Levandoski
panographic analysis in the diagnosis of hyperplasia of the coronoid process. Br J Oral
Stopa Z, Wanyura H, Kowalczyk P. Coronoid-condylar index in assessing of
oo
[102]
f
Maxillofac Surg 1999;37:409-411
pr
mandibular coronoid hyperplasia. Adv Med Sci 2013;58(2):429-433 LIST OF TABLES
Jo u
rn
al
Pr
e-
Table 1: Summary of case reports & case series included in this review
Page 22 of 36
Table 1: Summary of case reports & case series included in this review Authors/
Gend
Ons
Treatm
Typ
Associat
Treat
Surgic
Pre
Intr
Foll
Follo
Year
er
et
ent age
es
ed
ment
al
-op
a-
ow
w up
Age
(years)
approa
MO
op
up
perio
ch
(m
M
MO
d
m)
O
(m
(mont
(m
m)
hs)
history
(yea
oo
f
rs)
Schneble et
Ectom Male
NA
4
Bi
No
15
25
15
60
NA
NA
NA
NA
NA
IO
21
NA
NA
NA
IO
NA
NA
NA
12
IO
22
42
32
3
y
Fema et al/ 2018
NA
14
NA
30
Uni
[8] Ghazizadeh
Bi
Ribeiro da
15
Jo u
Male
rn
[9]
43
NA
Ectom
No
y
al
Male
No
Pr
le
e-
Tolentino
Silva et al/
NA
pr
al/ 2019 [7]
et al/2017
m)
Ectom Bi
NA y
2017 [10] Starch-
Jensen &
Male
Kjellerup/
NA
Ectom 18
Bi
No y
2017 [11]
Page 23 of 36
Romano et Ectom al/ 2017
Male
NA
37
Bi
No
IO
16
39
39
12
IO
20
38
40
12
13
41
39
12
EO
19
47
45
12
EO
13
38
43
12
EO
17
39
40
12
IO
15
NA
33
3
NA
NA
NA
NA
NA
y [12] Romano et Ectom al/ 2017
Male
NA
25
Bi
No y
[12] Romano et NA
43
Bi
No
IO
oo
Male
f
Ectom al/ 2017
y
Romano et
pr
[12]
Ectom
al/ 2017
Male
NA
27
Bi
No
e-
y
Romano et al/ 2017
Male
NA
29
Male
NA
Jo u
[12]
rn
Romano et al/ 2017
Bi
23
Bi
Ectom
No
al
[12]
Pr
[12]
y
Ectom No y
Acharya et al/ 2017 [13]
Male
13
Ectom 15.75
Bi
No y
Punyani & Fema Jasuja/
Ear 11
le
23
Uni
NA infection
2017 [14]
Page 24 of 36
Khandavilli Fema et al/ 2016
NA
16
Bi
NA
No Sx
No Sx
14
NA
NA
NA
NA
16
Bi
NA
No Sx
No Sx
10
NA
NA
NA
NA
0.25
Bi
No
le [15] Khandavilli Fema et al/ 2016 le [15] Monevska Ectom
f
Fema
IO
le
2
21
21
12
EO
5
10
NA
24
IO
20
41
41
12
No Sx
25
NA
NA
NA
IO
28
43
63
15
IO
32
35
65
18
IO
12
No
54
15
No Sx
15
NA
NA
NA
oo
et al/2016
y
[16] Pseudoca
pr
Balkin et
Ectom
al/ 2015
Male
0.59
2.17
Bi
mp
e-
y
todactyly
Choi et al/ Male
NA
31
2014 [18] Kim et al/ 13
Male
NA
Jo u
2014 [19]
rn
Kim et al/
43
Bi
21
No
Uni
No
15
y
No Sx
Ectom y
Kim et al/
Male
Ectom
No
Bi
al
Male 2014 [19]
Pr
[17]
Ectom 19
Bi
No
2014 [19]
y
Kim et al/
Ectom
Male
17.5
18
Uni
No
2014 [19]
y
Utsman et al/ 2013
Male
11
12
Bi
No
No Sx
[20]
Page 25 of 36
Sleeman et Fema al/ 2012
Ectom NA
7
Uni
Trauma
30 IO
le
15
y
NA
NA
3
[21] Newasker Ectom et al/ 2012
Male
NA
15
Uni
NA
EO
NA
NA
NA
6
Comb
23
NA
38
NA
21
30
NA
NA
20
NA
40
5
29
31
1
y [22] Ectom Male
NA
21
Uni
Trauma y
oo
2012 [23]
f
Bayar et al/
Robiony et
IO
Ectom Male
NA
NA
Bi
NA
(Endo
pr
al/ 2012
y
scope)
Costa et al/
Ectom
Male
NA
18
Bi
No
Pr
2012 [25] RamalhoFerreira et 23
Bi
2011[26]
Jo u
Peacock et Male
6
7
NA
y
Ectom
No
18. IO
y
rn
al/
26
al
Male
al/
e-
[24]
5
Ectom Uni
No
EO
16
40
38
6
EO
5
NA
35
18
NA
10
NA
28
NA
y
2011[27]
Galiѐ et al/
Fema
2010 [28]
le
NA
TMJ 3
Ectom
Uni arthrosis
y
Vaidhyanat Fema h & Raj/
Ectom NA
le
52
Bi
NA y
2010 [29]
Page 26 of 36
Iqbal et al/
Ectom Male
5
13
Uni
Trauma
2009 [30]
IO
30
NA
35
24
IO
30
50
43
15
IO
8
40
31
9
13
NA
40
12
IO
20
30
38
12
y
Yura et al/ Male
15
28
Uni
No
Otomy
2009 [31] Zhong et Fema al/ 2009
Ectom 26
39
Bi
No
le
y
f
[32]
oo
Fernández-
Ectom Ferro et al/
Male
NA
28
Bi
No
IO
y
pr
2008 [33] Gibbons & Abulhoul/
Male
16
36
Bi
e-
Ectom
NA
2007 [34] Mazzetto & Male
NA
Leovic et Male
17
Jo u
al/ 2006
rn
[35]
[36]
55
Bi
NA
No Sx
No Sx
32
NA
NA
NA
al
Hotta/ 2007
Pr
y
35
Bi
NA
Otomy
IO
15
NA
35
NA
Kursoglu & Capa/ 2006
Male
NA
24
Bi
No
No Sx
No Sx
27
NA
NA
NA
Male
NA
17
Bi
NA
No Sx
No Sx
14
NA
NA
NA
[37] Kursoglu & Capa/ 2006 [37]
Page 27 of 36
Satoh et al/
Ectom Male
12
13
Bi
No
2006 [38]
IO
27
40
45
8
IO
27
NA
6
42
IO
17
NA
40
72
y
Bertacci et al/ 2005
Male
15
25
Bi
No
Male
5
8
Bi
No
Otomy
[39] Mano et al/
Ectom y
f
2005 [40]
oo
Tieghi et
Ectom al/ 2005
Male
13
15
Bi
Trauma
IO
25
40
46
3
IO
25
40
40
20
IO
6
33
30
8
IO
21
NA
NA
18
IO
22
35
22
30
y
pr
[41] Tieghi et al/ 2005
Ectom
NA
17
Bi
le
e-
Fema
No
y
Pr
[41]
Abnorma
Fabie et al/
Fema le
Jo u
2002 [42]
8
swallowi
Ectom
Bi
rn
3
al
l
ng and
y
sucking reflex
Colquhoun et al/ 2002
Male
29
Ectom 32
Bi
No y
[43] Colquhoun Ectom et al/ 2002
Male
23
26
Bi
No y
[43]
Page 28 of 36
Gibbons et Ectom al/
Male
16
28
Bi
NA
EO
15
40
NA
NA
NA
25
NA
NA
NA
4
25
NA
NA
y 2001[44] Leonardi et al/
Male
NA
13
Bi
NBCCS
NA
2001[45] Moebius NA
1.5
Bi
syndrom
1999 [46]
f
Ectom Male
IO
8
oo
Turk et al/
NA
y e
pr
Moebius Turk et al/
Ectom
NA
NA
NA
Bi
IO
3010
y
40
e-
1999 [46]
syndrom
Loh et al/ Male
12
14
1997 [47] Loh et al/ NA
Loh et al/ Male
18
Jo u
1997 [47]
rn
1997 [47]
Loh et al/
Bi
22
Ectom
No
IO
13
22
32
12
IO
15
25
NA
NA
EO
5
20
NA
NA
IO
16
30
NA
NA
y Ectom
No y Ectom
Bi
No y
Fema
15
1997 [47]
41
Bi
al
Male
Pr
e
Ectom 25
Bi
No
le
y
Gerbino et
Male
14
15
Uni
No
Otomy
IO
15
NA
12
41
Male
15
32
Bi
NA
Otomy
IO
20
NA
60
42
al/ 1997 [5] Gerbino et al/ 1997 [5]
Page 29 of 36
Gerbino et Male
12
14
Uni
NA
Otomy
IO
12
NA
60
46
Male
10
13
Bi
NA
Otomy
IO
18
NA
15
40
Male
14
16
Bi
NA
Otomy
IO
20
NA
60
38
Male
30
40
Bi
No
IO
25
37
NA
NA
19
35
NA
NA
Comb
4
50
11
96
IO
21
NA
NA
NA
IO
23
38
32
14
IO
17
45
52
10
al/ 1997 [5] Gerbino et al/ 1997 [5] Gerbino et al/ 1997 [5] Ectom y
oo
1995 [48]
f
Currie et al/
Gibbons/
Ectom Male
17
34
Bi
No
IO
y
pr
1995 [49] Smyth & Wake/
Male
8
15
Bi
e-
Ectom
NA
1994 [50] Hönig et al/ Male
17
22
Uni
Fukumori
[52]
Male
14
23
Ectom
No
y
Short stature, Ectom
Bi
blepharo y
Jo u
et al/ 1993
rn
al
1994 [51]
Pr
y
chlasis
Totsuka & Fukuda/
Male
14
Ectom 17
Bi
No y
1991[53]
Page 30 of 36
Totsuka & Ectom Fukuda/
Male
10
13
Bi
No
IO
29
48
45
3
EO
22
NA
40
12
y 1991[53] Hayter & Ectom Robertson/
Male
15
16
Bi
No y
1989 [54] Shultz & 14
16
Bi
No
IO
20
40
48
24
IO
10
34
38
12
Comb
9
35
37
24
IO
14
45
37
3
oo
Male
f
Ectom Theisen/
y
Hall et
pr
1989 [55]
Ectom
al/1989
Male
12
23
Bi
No
e-
y
Hall et al/1989
Male
21
24
Macleod/ 1987 [57] Macleod/
14
Bi
Ectom
No
y
Ectom No y
NA
15
Bi
No
No Sx
No Sx
18
NA
NA
NA
Male
NA
17
Bi
No
No Sx
No Sx
20
NA
NA
NA
Male
NA
66
Bi
Trauma
IO
9
41
26
3
IO
38
60
45
3
Jo u
Male
NA
rn
Male
Bi
al
[56]
Pr
[56]
1987 [57] Macleod/
1987 [57] Macleod/
Ectom
1987 [57]
y
Macleod/
Ectom Male
1987 [57]
NA
47
Uni
Trauma y
Page 31 of 36
Giacomuzz
Arm Male
11
19
Bi
i/ 1986 [58]
No Sx
No Sx
11
NA
NA
NA
exostosis
Bronstein & Osborne/
Male
NA
20
Bi
Trauma
Otomy
IO
20
30
39
3
Male
NA
29
Bi
No
No Sx
No Sx
26
NA
NA
NA
44
54
Bi
No
1985 [59]
Gallimore/
f
Balcunas &
oo
1985 [60] Kreutz &
Ectom
le
le
17
18
No
Bi
14
Jo u
[64]
rn
Tucker et Male
45
24
IO
14
43
27
11
IO
15
NA
40
3
16
Uni
EO
22
40
44
3
IO
13
28
30
3
IO
10
NA
NA
NA
y
Ectom
No
al
[63]
Bi
Pr
38
Praal/1984
al/ 1984
50
Ectom
NA
Male
e-
Fema
1985 [62]
16
y
1985 [61] Kraut/
EO
pr
Fema Sanders/
y
Ectom No y
Bernstein &
Male
NA
Ectom 17
Bi
No
Fernandez/
y
1984 [65] York & Fema Cockerham
Ectom 6
le
7
Bi
No y
/ 1983 [66]
Page 32 of 36
York & Fema Cockerham
Ectom 11
12
Bi
No
le
IO
10
NA
NA
NA
IO
14
45
36
NA
NA
22
NA
NA
5
y
/ 1983 [66] Marra/
Ectom Male
NA
13
Bi
No
1983 [67]
y
Lucaya et Fema
Ectom 8.67
9
Uni
No
le
y
24.3 Male
1981[69]
Ectom 25
Uni
Trauma
3
Duffy et al/ 15
Bi
NA
41
3
IO
8
30
NA
NA
IO
16
48
NA
IO
12
35
28
3
Comb
9
30
40
8
IO
8
20
37
144
Male
14
16
Bi
Male
23
Jo u
1979 [72]
rn
Shuken &
Male
NA
38
Bi
Ectom y
Ectom 19
Uni
No y Difficult
Monks/
NA
y
No
1979 [73]
Male
Ectom
No
al
1980 [71]
Pr
y
Hecker &
Rivas/
No
e-
NA
1980 [70]
Girard/
11
Ectom
Male
Corwin/
IO
y
pr
Javid/
oo
[68]
f
al/ 1982
Ectom 50
Bi
extractio
1978 [74]
y n
Page 33 of 36
Michel et Fema al/ 1977
Ectom NA
30
Uni
No
le
IO
10
NA
NA
NA
IO
11
31
12
46
NA
22
NA
45
NA
y
[75] Kallioniemi Fema et al/ 1975
Ectom 15
20
Uni
No
le
y
[76] Ectom Male
NA
44
Bi
Trauma y
oo
1975 [77]
f
Shurman/
Scott &
Ectom Male
NA
25
Bi
No
EO
15
37
28
3
Otomy
IO
18
NA
38
7
No Sx
No Sx
13
NA
NA
NA
EO
9
NA
18
32
No Sx
17
NA
NA
NA
pr
Frew/ 1975
y
e-
[78] Mild
Brusati/
torticolli
Male
12
21
Bi
NA
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Male
rn
van Hoof & Besling/
s,
juvenile
al
1974 [79]
Pr
Rusconi &
diabetes
12
Bi
No
20
Bi
No
1973 [80]
van Hoof & Besling/
Male
NA
Ectom y
1973 [80] van Hoof & Besling/
Male
NA
46
Bi
No
No Sx
1973 [80]
Page 34 of 36
van Hoof & Ectom Besling/
Male
10
15
Bi
No
IO
24
42
6
42
IO
17
NA
NA
NA
y 1973 [80] van Hoof & Ectom Besling/
Male
NA
18
Uni
Trauma y
1973 [80] van Hoof & NA
18
Bi
No
NA
18
43
2
33
IO
17
35
NA
NA
Comb
10
NA
NA
NA
EO
11
35
6
35
IO
5
22
40
24
Comb
9
20
24
1
IO
14
45
NA
NA
oo
Male
f
Ectom Besling/
y
Bramley &
pr
1973 [80]
Ectom
Norman/
Male
19
24
Uni
No
e-
y
Muldoon/ Male
14
17
1971 [82]
Pr
1972 [81]
Bi
Ectom
Trauma
y
Male
13
Fitzpatrick/
18
Jo u
Male
22
rn
[83]
al
Right
Hurd/ 1970
27
Uni
Ectom TMJ y clicking Ectom
Bi
No
1970 [84]
y
Nickerson
et al/ 1969
Male
12
Ectom 22
Bi
No y
[85] Allison et Ectom al/ 1969
Male
15
18
Bi
No y
[86]
Page 35 of 36
Rowe/
Ectom Male
12
15
Bi
No
1963 [87]
IO
15
NA
35
14
No Sx
10
NA
NA
NA
y
Rowe/ Male
13
15
Bi
No
No Sx
1963 [87]
Jo u
rn
al
Pr
e-
pr
oo
f
Uni= Unilateral, Bi= Bilateral, Ectomy= Coronoidectomy, Otomy= Coronoidotomy, No Sx= No Surgery, IO= Intraoral, EO= Extraoral, Comb= Combined intraoral & extraoral, NA= not available
Page 36 of 36
PII:
S2468-7855(19)30305-2
DOI:
https://doi.org/doi:10.1016/j.jormas.2019.12.019
Reference:
JORMAS 789
To appear in:
Journal of Stomatology oral and Maxillofacial Surgery
Received Date:
9 October 2019
Accepted Date:
18 December 2019
Please cite this article as: Goh YC, Tan CC, Lim D, Coronoid Hyperplasia: A Review, Journal of Stomatology oral and Maxillofacial Surgery (2020), doi: https://doi.org/10.1016/j.jormas.2019.12.019
This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Published by Elsevier.
CORONOID HYPERPLASIA: A REVIEW Yet Ching Goh Department of Oral and Maxillofacial Clinical Sciences, Faculty of Dentistry, University of Malaya, 50603 Kuala Lumpur, Malaysia Chuey Chuan Tan
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Department of Oral and Maxillofacial Clinical Sciences,
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Faculty of Dentistry, University of Malaya,
Daniel Lim
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50603 Kuala Lumpur, Malaysia
Faculty of Dentistry, University of Malaya,
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50603 Kuala Lumpur, Malaysia
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Department of Oral and Maxillofacial Clinical Sciences,
Corresponding author Dr Daniel Lim
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Department of Oral and Maxillofacial Clinical Sciences, Faculty of Dentistry, University of Malaya,
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50603 Kuala Lumpur, Malaysia.
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Tel No.: +603-79674807
Fax No.: +603-79674534
E-mail: [email protected] Disclosure of interest
The authors declare that they have no competing interest ABSTRACT Coronoid hyperplasia is one of the rare causes of progressive limitation of mouth opening due to impingement of the enlarged coronoid process of the mandible on the zygomatic bone. A
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review was performed on all cases reports and case series on coronoid hyperplasia. Gender, age at treatment, age of onset, types of hyperplasia (unilateral/bilateral), associated history, treatment, surgical approach, pre-operative mouth opening, intra-operative mouth opening, mouth opening at follow up and follow up period were recorded and analyzed. A total of 82 articles which reported 115 cases were included. Coronoid hyperplasia was commonly reported at mean age of 22.64 years
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old with male preponderance. Most of the cases were diagnosed and treated between the age of
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11-20 years old. This condition commonly involved bilateral coronoid process of mandible. The mean width of pre-operative mouth opening was 16.5mm and was improved to a mean mouth
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opening of 36.3mm intra operatively. Mean mouth opening was 34.8mm at an average follow up
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of 19 months. While the etiopathogenesis of coronoid hyperplasia is still not conclusive, treatment
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with either coronoidectomy or coronoidotomy produced good improvement in mouth opening. Keywords: mandible; coronoid process; hyperplasia; elongation; enlargement
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1. INTRODUCTION
The temporomandibular joint (TMJ) is a complex joint which provides articulation
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between the fixed temporal bone of the cranium and the movable mandible. The TMJs are bilateral,
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diarthrodial, lined by synovial membrane and freely movable joints [1]. Besides mandibular condyle, coronoid process is the other process that is attached to the ramus of mandible. This “crown-like” process of the mandible serves mainly as the attachment for temporalis muscle and partly for masseter muscle on its lateral surface. Aside from this, coronoid process does not have other role in the function of the jaw. Because of this, coronoid process can be removed either as a source of bone graft or as a result of pathology without posing any functional issues. This accessory process of the mandible can be either of triangular, rounded or hook shaped. Majority of the process are of triangular shape (49% - 67%), followed by hook shaped (21% - 30%) and the
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rounded process (3% - 24.58%) [2]. The length of coronoid process ranges from 13.9mm to 15.3mm with the right side longer than the left. The length is not affected by gender [3]. Coronoid process enlargement is relatively uncommon, and this condition leads to impingement of the coronoid process on the zygomatic bone restricting mandibular opening [4-6]. It can either be a true hyperplasic phenomenon or due to the presence of pathology lesions [4]. Coronoid process
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hyperplasia is an abnormal elongation of the mandibular coronoid process consisting of
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histologically normal bone [6]. Progressive reduction of mouth opening is the most consistent symptom [4,5]. The etiology of coronoid process hyperplasia is unclear to date, but several theories
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have been suggested [4,5]. This paper aims to provide a summary of reported cases of coronoid
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hyperplasia with regards to demographic details, etiopathology, clinical features and outcome from
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the treatments provided. 2. METHODS
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We performed this review with the intention to summarize findings from all the available literatures to provide an update on coronoid hyperplasia. PubMed and EBSCO database were used
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to search for relevant articles. In the search, the following keywords were used ‘coronoid’ and
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‘hyperplasia’. For the term ‘coronoid’, synonyms ‘coronoid process’ was entered. For term ‘hyperplasia’, synonyms ‘enlargement’ and ‘elongation’ were entered. Boolean operator OR was applied between synonyms and operator AND was used between the two search terms. This review included all case reports and case series in English language found in PubMed and EBSCO using the search terms. No limit was imposed on the publication year. Assessment of the titles and abstracts were carried out to select relevant articles. Reference lists of the selected articles were checked to trace additional articles that are not found in both PubMed and EBSCO.
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Full texts of the relevant articles were then retrieved either through online databases or hand search. Cases with histopathology and/or morphology of osteochondroma were excluded. Data extracted from the included articles were gender, age at treatment, age of onset, types of hyperplasia (unilateral/bilateral), associated history, treatment, surgical approach, pre-operative mouth opening, intra-operative mouth opening, mouth opening at follow up and duration of follow
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up. Descriptive analysis was employed. Data analysis were completed using SPSS version 24. 3. RESULTS
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Literature search was performed on the 15th July 2019. A total of 742 articles were obtained
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from both PubMed and EBSCO. After removing duplicates, non-relevant articles and osteochondroma cases, a total of 82 articles reporting 115 cases were included in this review (Table
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1).
The mean reported age at diagnosis was 22.64 years old. The youngest patient reported
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was 0.25 years old while the oldest patient was 66 years old. Majority (42.6%, n=49) of the patients
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were in the age group of 11 to 20 years old followed by age group of 21 to 30 years old (26.1%, n=30). On the other hand, the mean onset age was 14.7 years old. Similar to the age at diagnosis,
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majority of the patients’ age of onset was between 11 to 20 years old. However, as many as 52 articles failed to provide history of onset of the disease. From this review, it is evident that coronoid hyperplasia was of male preponderance, with male to female ratio of 5:1. Hyperplasia of both coronoid processes were the most reported, representing 79.1% of the reported cases, while the rest were unilateral cases. While most of the cases were idiopathic (66.1%, n=76), considerable amount of cases (9.6%, n=11) were attributed to previous history of trauma. Other less common histories were temporomandibular joint disorders, Moebius Syndrome, mild torticollis, nevoid
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basal cell carcinoma of skin, pseudocamptodactyly, ear infection and even difficult dental extraction. Progressive reduction of mouth opening is the hallmark of coronoid hyperplasia. The range of mouth opening in patients affected by coronoid hyperplasia was between 2mm-38mm. Generally, the mean pre-operative mouth opening was 16.5mm. However, it is worth mentioning
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that pre-operative mouth opening was not reported in 4 cases. On the other hand, intra-operative
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mouth opening averaged at 36.3mm with the range of 10mm-60mm. Almost half (45.2%, n=52)
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of the literature did not report their intra-operative achievements. As there is no proper follow-up guideline available, the range of follow-up period differed from as short as 1 month to the longest
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144 months. The mean follow-up period was around 19 months. Follow-up protocol was not
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mentioned in 44 cases. In 73 cases, the authors recorded the final width of mouth opening at the end of their follow-up. This width ranged from as low as 2mm to as high as 65mm. The mean final mouth opening was 34.8mm, which was almost the same as the mouth opening achieved during
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surgery. Apart from limited mouth opening, facial asymmetry and temporomandibular joint
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disorders were other more commonly reported signs and symptoms.
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There are mainly two types of surgical treatment provided. Coronoidectomy was performed in 76.5% (n=88) of the cases while coronoidotomy was performed in 8.7% (n=10) of the cases. No surgery was performed in 14 cases either due to age factor or patients were not keen for treatment. However, details of treatment provided were not mentioned in 3 cases. Intraoral approach was the preferred approach as it was used in 61.7% (n=71) of the cases. Extraoral approach was only used in a small number of patients (13%, n=15). To gain better access, surgeons performed surgery via both intraoral and extraoral approaches in 6 patients. Only one group of authors reported the use of endoscope via intraoral approach while performing coronoidectomy.
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4. DISCUSSION Till date, pathogenesis of coronoid hyperplasia remains unknown. As a result, various hypotheses had been put forward to explain the pathogenesis. As with most other diseases, role of genes in the pathogenesis was coined by various authors following cases that were encountered. van Hoof and Besling observed bilateral coronoid hyperplasia in patients with trismus-
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pseudocamptodactyly syndrome [80]. This syndrome is inherited in an autosomal dominant
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fashion. Hecht and Beals also reported similar presentation in their patients [88]. Veugelers et al
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did a sequence analysis on large kindred affected by trismus-pseudocamptodactyly syndrome and found a mutation of MYH8 gene. This gene encodes for class II myosin heavy chains which is
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important for skeletal muscle contraction [89]. In 2002, Leonardi et al reported the occurrence of
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coronoid hyperplasia in patients with nevoid basal cell carcinoma syndrome which may suggest possible genetic role in development of coronoid hyperplasia [90]. Apart from association with other diseases, coronoid hyperplasia was also reported in a pair of identical twins. This report
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further convinces the genetic basis hypotheses [5]. This review shows most of the cases involved
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both sides of coronoid process. This reflects a possible systemic effect governs by genetic factors
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rather than local factors. However, more studies are needed to prove this association. Role of hormone had also been associated with coronoid hyperplasia. This was coined by Rowe in 1963 as he observed this condition in two of his patients who presented to him at the age of 15 [87]. However, the role of hormone was not favored due to lack of evidence. Echoing Rowe’s idea, in this review, we observed that most of the patients presented between the age of 11-20 years old coinciding with the normal growth spurt. Thus, we felt that further studies on hormonal role in coronoid hyperplasia are necessary.
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Coronoid hyperplasia was also thought to be associated with temporomandibular disorders. It is commonly seen together with untreated temporomandibular joint ankylosis. In this condition, there is complex muscular interactions between the elevator and depressor muscles of the jaw trying to maintain normal jaw function. As a result of this, temporalis muscle undergoes hyperemia, atrophy and eventually fibrosis. Due to its myostatic contracture state, fibrosed tendon
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of temporalis muscle causes hyperactivity of the suprahyoid muscles during mouth opening. In
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turn, the suprahyoid muscles induce isometric contraction of temporalis muscle due to the function of mandibular reciprocal inhibition [91,92]. Ultimately, hyperplasia or elongation of the coronoid
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process occurs under the contraction force of temporalis muscle akin to distraction osteogenesis
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[93]. While Farrar and McCarty suggested that coronoid hyperplasia maybe related to existing temporomandibular joint disorders [94], Isberg et al specifically linked it with prolonged
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temporomandibular joint disc displacement [95]. It is important to note that both coronoid hyperplasia and chronic TMJ disc displacement produce almost similar clinical presentation which
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are progressive limitation of mouth opening with ipsilateral jaw deviation, in unilateral cases. This
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renders initial diagnosis challenging, especially borderline cases, without radiographic investigations. It was observed that some cases were initially diagnosed with TMJ disorders
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following patients’ clinical presentations; but were later diagnosed as coronoid hyperplasia following radiographic findings. Their signs and symptoms were relieved following treatment of the hyperplastic coronoid process. In connection with TMJ disorders, Wenghoefer et al in 2008 reported coronoid hyperplasia in patients with ankylosing spondylitis. Although they believed that TMJ can be affected similar to the sacroiliac joint, but they were unable to prove this under the microscope [96].
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Some authors attributed coronoid hyperplasia to previous facial trauma. Trauma to the zygoma [23,30] and mandible [21,41] had been reported so far. It was postulated that following facial trauma, tensile forces of the temporalis muscle exerted on the coronoid process was akin to distraction osteogenesis leading to elongation of the process [23]. On the other hand, Smyth and Wake were of the opinion that coronoid process hyperplasia occurred following torn temporalis
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tendon near its insertion which lead to hematoma formation and subsequent clot organization
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leading to new bone forming at the coronoid [50].
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The role of temporalis muscle activity cannot be disregarded in the pathogenesis of coronoid hyperplasia as it is the main structure that attaches to the coronoid process. Sarnat and
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Engel back in 1951, proposed that hyperactivity of temporalis muscle could be the cause of
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coronoid hyperplasia [97]. Jamal et al reported that contralateral coronoid process showed elongation following hemimandibulectomy with disarticulation [98]. In these cases, loss of half of the mandible possibly led to increased muscular activity of the contralateral temporalis as the jaw
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elevator. Prolonged increased muscular pull on the coronoid might lead to its elongation. Puche et
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al hypothesized the role of congenital hypotonia in the development of coronoid hyperplasia. They
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believed that reduced mandibular movements and deglutition could have led to relative hyperactivity of temporalis muscle which was not counterbalanced by infra and suprahyoid muscles may be the cause of coronoid hyperplasia in two of their patients [99]. However, Gerbino et al and Hall et al refuted the role of hyperactive temporalis muscle. Their rebuttals were supported by normal electromyography findings in their patients with hyperplastic coronoid [5,56]. Although none of the hypotheses mentioned have strong evidence to support them, we can notice that most of these hypotheses suggested a crucial role of temporalis muscle in the pathogenesis of coronoid hyperplasia either directly or indirectly.
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In most of the operated cases, coronoidectomy was the treatment of choice. This procedure involves removal of the osteotomized coronoid process. Prior to completion of the osteotomy, some authors tied a stainless-steel wire to the coronoid process through a hole made using round bur or to a screw anchored to the coronoid process while others held it with forceps [12,53]. This was to avoid the osteotomized coronoid process from being pulled superiorly by temporalis muscle
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rendering subsequent removal more challenging. A few authors performed coronoidotomy by
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leaving the coronoid segment in-situ following osteotomy. Advocators of this techniques reported good outcome as the hyperplastic coronoid process had been separated from the rest of the
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mandible making its movements unhindered by the zygomatic bone [5,31]. Besides that,
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coronoidotomy also requires less tissue reflection therefore reducing tissue damage and scarring. Despite simplicity of this technique, it comes with the risk of coronoid process reunion with the
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ramus [31]. To overcome this risk, Chen et al performed modified (gap) coronoidotomy which involved removal of a strip of bone from the base of coronoid process thus creating a gap of 5-
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6mm between coronoid process and ramus [100]. Mulder and his colleagues summarized in their
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review that coronoidotomy had better post-operative results, although not significant, compared to coronoidectomy despite the latter being treatment of choice [6]. Access to the coronoid process
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can be achieved either via intraoral or extraoral approaches. The choice of approach depends on the amount of mouth opening and surgeon’s experience. Extraoral approach is preferred if the limitation of mouth opening is severe. Among the extraoral approaches used were submandibular, pre-auricular and coronal approaches. Exposure of coronoid process is hindered by severe limitation of mouth opening. By using extraoral approach, complete coronoidectomy and myotomy, fasciotomy and zygomatic osteotomy can be performed. However, intraoral approach was more preferred due to the possible risk of facial nerve injury and external scar with extraoral
Page 9 of 36
approach. In an intraoral approach, incision is made along the external oblique ridge followed by stripping of temporalis muscle fibers from coronoid process prior to osteotomy. Robiony et al performed endoscopically assisted coronoidectomy in their patients and claimed the technique had less morbidity, faster and allow physical therapy to be started sooner [24]. Regardless of the types of treatment provided, post-operative physiotherapy plays a very
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important role in at least maintaining, if not improving, the width of mouth opening achieved
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during the surgery. Physiotherapy can be performed using spatulas, mouth screw, dynamic
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devices, wedge or Therabite® device. Although there was no study to compare which device is more superior for physiotherapy in coronoid hyperplasia, some authors advocated the use of
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Therabite® device as it is easy to use [34]. Its horseshoe-shaped surfaces are in contact with
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multiple anterior and posterior teeth, making it more comfortable and less stress on anterior teeth compared to spatulas and mouth screw. Spatulas and mouth screws are usually wedged between the upper and lower anterior teeth. Many authors advocated that aggressive physiotherapy must be
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performed during the first year of surgery.
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Dental panoramic tomography (DPT) was the most commonly used imaging modality to
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assist in the diagnosis of coronoid hyperplasia. Instead of using an absolute normal value of coronoid length as reference, Kubota et al in 1999 utilized Levandoski panographic analysis to aid in diagnosis of coronoid hyperplasia. They measured coronoid-gonion and condyle-gonion distances based on dental panoramic tomogram. Ratio of coronoid-gonion to condyle-gonion was later computed and they concluded a mean ratio of 0.94 was considered normal as opposed to 1.17 in diseased group. They suggested that patients with limited mouth opening and coronoidgonion:condyle-gonion ratio above 1.1 are likely to have coronoid hyperplasia [101]. However, it should be highlighted that these values were derived from a small group of 3 subjects with coronoid
Page 10 of 36
hyperplasia. With the availability of computed tomography, not only the hyperplastic coronoid process can be visualized but also its shape and its actual relation between coronoid process and the zygoma. Stopa and his colleagues later in 2013 measured the similar distances but based on 3D reconstruction of computed tomography scan. A ratio of up to 1.07 was considered as normal while ratio above 1.15 signified possibility of coronoid hyperplasia [102]. By using these methods
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of measurement, condition of the condyle has a great impact on the ratio. Any abnormalities in
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condylar length will give a false impression on the coronoid process.
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5. CONCLUSION
From this review, it can be observed that coronoid hyperplasia was mainly seen in the
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second decade of life and predominantly in male. It was commonly presented as bilateral cases.
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Despite the controversial etiologies, this condition can be treated with either coronoidectomy or coronoidotomy producing satisfactory outcome. However, it must be highlighted that the above
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inferences are made based on data available in the literatures included.
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REFERENCES
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[1] David CM, Elavarasi P. Functional anatomy and biomechanics of temporomandibular joint and the far-reaching effects of its disorders. J Adv Clin Res Insights 2016;3:101-106 [2] Tapas S. Morphological variations of coronoid process in dry adult human mandibles. Indian Journal of Basic and Applied Medical Research 2014;3(2):401-405 [3] Nayak S, Patra S, Singh G, Mohapatra C, Rath S. Study of the size of the coronoid process of mandible. IOSR Journal of Dental and Medical Sciences 2015;14(6):66-69
Page 11 of 36
[4] McLoughlin PM, Hopper C, Bowley NB. Hyperplasia of the mandibular coronoid process: An analysis of 31 cases and a review of literature. J Oral Maxillofac Surg 1995;53:250255 [5] Gerbino G, Bianchi SD, Bernardi M, Berrone S. Hyperplasia of the mandibular coronoid process: long-term follow-up after coronoidotomy. J Craniomaxillofac Surg 1997;25:169-
f
173
oo
[6] Mulder CH, Kalaykova SI, Gortzak RA Th. Coronoid process hyperplasia: a systematic review of the literature from 1995. Int J Oral Maxillofac Surg. 2012;41:1483-1489
pr
[7] Schneble EJ, Moore RD, Pettersson DR, Pollock JM, Barajas RF, Jr. Coronoid Process
e-
Hyperplasia : A Rare Disorder Masquerading as Temporomandibular Joint Disease. Clin Neuroradiol. 2019
Pr
[8] Tolentino MCA, Assis JS, Cardoso CAeA, Manzi FR. Mandibular coronoid process hyperplasia: a case report. Rev CEFAC 2018;20(3):400-405
al
[9] Ghazizadeh M, Sheikhi M, Salehi MM, Khaleghi A. Bilateral coronoid hyperplasia causing
[10]
rn
painless limitation of mandibular movement. Radiol Case Rep. 2018;13(1):112-117 Ribeiro da Silva J, Pereira RDS, Agueda C, Nunes PM, Marin C, Hochuli-Vieira
Jo u
E. Bilateral Coronoid Hyperplasia in a 43-Year-Old Patient Treated With Intraoral Coronoidectomy. J Craniofac Surg. 2017;28(4):e402-e403 [11]
Starch-Jensen T, Kjellerup AD. Bilateral Elongated Mandibular Coronoid Process
and Restricted Mouth Opening: A Case Report. Open Dent J. 2017;11:670-678 [12]
Romano M, Porcellini G, Rossi D, Bolzoni A, Gianni AB, Silvestre FJ, et al.
Bilateral coronoid hyperplasia: a report of six cases. J Biol Regul Homeost Agents. 2017;31(2 Suppl 1):139-145
Page 12 of 36
[13]
Acharya P, Stewart A, Naini FB. Coronoid impingement syndrome: literature
review and clinical management. Maxillofac Plast Reconstr Surg. 2017;39(1):11 [14]
Silky R Punyani VRJ. Unilateral acquired condylar hypoplasia and coronoid
hyperplasia of the mandible. 2017;10:198-201 [15]
Khandavilli SD, Pattni N, Naredla PR, Williams R. First case of bilateral coronoid
f
hyperplasia in monozygotic twin sisters-a new aetiological perspective? Oral Maxillofac
[16]
oo
Surg. 2016;20(4):441-443
Monevska DP, Benedetti A, Popovski V, Naumovski S, Grcev A, Bozovic S, et al.
pr
Mandibular Movement Restoration in a Child with Bilateral Coronoid Hyperplasia: A Case
[17]
e-
Report. Open Access Maced J Med Sci. 2016;4(2):293-295
Balkin DM, Chen I, Oberoi S, Pomerantz JH. Bilateral Coronoidectomy by
2015;26(6):1954-1956
Choi MG, Kim DH, Ki EJ, Cheon HM. Trismus Due to Bilateral Coronoid
al
[18]
Pr
Craniofacial Approach for Hecht Syndrome-Related Trismus. J Craniofac Surg.
[19]
rn
Hyperplasia. Maxillofac Plast Reconstr Surg. 2014;36(4):168-172 Kim SM, Lee JH, Kim HJ, Huh JK. Mouth opening limitation caused by coronoid
Jo u
hyperplasia: a report of four cases. J Korean Assoc Oral Maxillofac Surg. 2014;40(6):301307 [20]
Utsman RA, Klasser GD, Padilla M. Coronoid hyperplasia in a pediatric patient:
case report and review of the literature. J Calif Dent Assoc. 2013;41(10):766-770 [21]
Sleeman D, Warren E, McAuliffe M. Unilateral coronoid hyperplasia associated
with early childhood facial trauma: a case presentation. J Ir Dent Assoc. 2012;58(4):212214
Page 13 of 36
[22]
Newaskar V, Idrees F, Patel P. Unilateral coronoid hyperplasia treated by
coronoidectomy using a transzygomatic approach. Natl J Maxillofac Surg. 2012;3(2):195198 [23]
Bayar GR, Akcam T, Gulses A, Sencimen M, Gunhan O. An excessive coronoid
hyperplasia with suspected traumatic etiology resulting in mandibular hypomobility.
Robiony M, Casadei M, Costa F. Minimally invasive surgery for coronoid
oo
[24]
f
Cranio. 2012;30(2):144-149
hyperplasia: endoscopically assisted intraoral coronoidectomy. J Craniofac Surg.
Costa YM, Porporatti AL, Stuginski-Barbosa J, Cassano DS, Bonjardim LR, Conti
e-
[25]
pr
2012;23(6):1838-1840
Dent J. 2012;23(3):252-255 [26]
Pr
PC. Coronoid process hyperplasia: an unusual cause of mandibular hypomobility. Braz
Ramalho-Ferreira G, Faverani LP, Fabris AL, Pastori CM, Magro-Filho O, Ponzoni
al
D, et al. Mandibular movement restoration through bilateral coronoidectomy by intraoral
[27]
rn
approach. J Craniofac Surg. 2011;22(3):988-991 Peacock ZS, Resnick CM, Faquin WC, Kaban LB. Accessory mandibular condyle
Jo u
at the coronoid process. J Craniofac Surg. 2011;22(6):2168-2171 [28]
Galie M, Consorti G, Tieghi R, Denes SA, Fainardi E, Schmid JL, et al. Early
surgical treatment in unilateral coronoid hyperplasia and facial asymmetry. J Craniofac Surg. 2010;21(1):129-133 [29]
Vaidhyanath R, Raj V. Mandibular coronoid process hyperplasia causing restricted
mouth opening. Br J Hosp Med (Lond). 2010;71(4):229
Page 14 of 36
[30]
Iqbal S, Hamid ALA, Purmal K. Unilateral coronoid hyperplasia following trauma:
a case report. Dental Traumatology. 2009;25(6):626-630 [31]
Yura S, Ohga N, Ooi K, Izumiyama Y. Mandibular coronoid hyperplasia: a case
report. Cranio. 2009;27(4):275-279 [32]
Zhong SC, Xu ZJ, Zhang ZG, Zheng YH, Li TX, Su K. Bilateral coronoid
f
hyperplasia (Jacob disease on right and elongation on left): report of a case and literature
[33]
oo
review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2009;107(3):e64-e67 Fernandez Ferro M, Fernandez Sanroman J, Sandoval Gutierrez J, Costas Lopez A,
pr
Lopez de Sanchez A, Etayo Perez A. Treatment of bilateral hyperplasia of the coronoid
e-
process of the mandible. Presentation of a case and review of the literature. Med Oral Patol Oral Cir Bucal. 2008;13(9):E595-E598
Gibbons AJ, Abulhoul S. Use of a Therabite appliance in the management of
Pr
[34]
bilateral mandibular coronoid hyperplasia. Br J Oral Maxillofac Surg. 2007;45(6):505-506 Mazzetto MO, Hotta TH. Hypertrophy of the mandibular coronoid process and
al
[35]
rn
structural alterations of the condyles associated with limited buccal opening: case report. Braz Dent J. 2007;18(2):171-174 Leovic D, Djanic D, Zubcic V. Mandibular locking due to bilateral coronoid
Jo u
[36]
process hyperplasia. Wien Klin Wochenschr. 2006;118(19-20):594 [37]
Kursoglu P, Capa N. Elongated mandibular coronoid process as a cause of
mandibular hypomobility. Cranio. 2006;24(3):213-216 [38]
Satoh K, Ohno S, Aizawa T, Imamura M, Mizutani H. Bilateral coronoid
hyperplasia in an adolescent: report of a case and review of the literature. J Oral Maxillofac Surg. 2006;64(2):334-338
Page 15 of 36
[39]
Bertacci A, Landi N, Manfredini D, Ferronato G, Bosco M. Coronoid hyperplasia.
A case report. Minerva Stomatol. 2005;54(7-8):461-470 [40]
Mano T, Ueyama Y, Koyama T, Nishiyama A, Matsumura T. Trismus due to
bilateral coronoid hyperplasia in a child: case report. J Oral Maxillofac Surg. 2005;63(3):399-401 Tieghi R, Galie M, Piersanti L, Clauser L. Bilateral hyperplasia of the coronoid
f
[41]
[42]
oo
processes: clinical report. J Craniofac Surg. 2005;16(4):723-726
Fabie L, Boutault F, Gas C, Paoli JR. Neonatal bilateral idiopathic hyperplasia of
Colquhoun A, Cathro I, Kumara R, Ferguson MM, Doyle TC. Bilateral coronoid
e-
[43]
pr
the coronoid processes: case report. J Oral Maxillofac Surg. 2002;60(4):459-462
hyperplasia in two brothers. Dentomaxillofac Radiol. 2002;31(2):142-146 Gibbons AJ, Byrne AJ, Key SJ. Trismus due to bilateral mandibular coronoid
Pr
[44]
hyperplasia. J R Army Med Corps. 2001;147(3):311-313 Leonardi R, Sorge G, Caltabino M. Bilateral hyperplasia of the mandibular
al
[45]
rn
coronoid processes associated with the nevoid basal cell carcinoma syndrome in an Italian boy. Br Dent J. 2001;190(7):349-350 Turk AE, McCarthy JG, Nichter LS, Thorne CH. Moebius syndrome: the new
Jo u
[46]
finding of hypertrophy of the coronoid process. J Craniofac Surg. 1999;10(1):93-96 [47]
Loh HS, Ling SY, Lian CB, Shanmuhasuntharam P. Bilateral coronoid hyperplasia-
-a report with a view on its management. J Oral Rehabil. 1997;24(10):782-787 [48]
Currie WJ, Stassen LF, Thompson WD. An unusual cause of trismus. Dent Update.
1995;22(2):72-73
Page 16 of 36
[49]
Gibbons AJ. Case report: Computed tomography in the investigation of bilateral
mandibular coronoid hyperplasia. Br J Radiol 1995;68:531-533 [50]
Smyth AG, Wake MJ. Recurrent bilateral coronoid hyperplasia: an unusual case.
Br J Oral Maxillofac Surg. 1994;32(2):100-104 [51]
Honig JF, Merten HA, Korth OE, Halling F. Coronoid process enlargement.
Fukumori T, Tagawa T, Inui M. Bilateral coronoid process hyperplasia and short
oo
[52]
f
Dentomaxillofac Radiol. 1994;23(2):108-110
stature. A case report. Int J Oral Maxillofac Surg. 1993;22(3):139-144 Totsuka Y, Fukuda H. Bilateral coronoid hyperplasia. Report of two cases and
pr
[53]
[54]
e-
review of the literature. J Craniomaxillofac Surg. 1991;19(4):172-177 Hayter JP, Robertson JM. Surgical access to bilateral coronoid hyperplasia using
[55]
Pr
the bicoronal flap. Br J Oral Maxillofac Surg. 1989;27(6):487-493 Shultz RE, Theisen FC. Bilateral coronoid hyperplasia. Report of a case. Oral Surg
Hall RE, Orbach S, Landesberg R. Bilateral hyperplasia of the mandibular coronoid
rn
[56]
al
Oral Med Oral Pathol. 1989;68(1):23-26
processes: a report of two cases. Oral Surg Oral Med Oral Pathol. 1989;67(2):141-145 Macleod AW. Limitation of mandibular opening due to enlarged coronoid
Jo u
[57]
processes. Aust Dent J. 1987;32(2):120-125 [58]
Giacomuzzi D. Bilateral enlargement of the mandibular coronoid processes: review
of the literature and report of case. J Oral Maxillofac Surg. 1986;44(9):728-731 [59]
Bronstein SL, Osborne JJ. Mandibular limitation due to bilateral coronoid
enlargement: management by surgery and physical therapy. Cranio. 1985;3(1):58-62
Page 17 of 36
[60]
Balcunas BA, Gallimore R. Bilateral coronoid hyperplasia. Dentomaxillofac
Radiol. 1985;14(1):41-44 [61]
Kreutz RW, Sanders B. Bilateral coronoid hyperplasia resulting in severe limitation
of mandibular movement. Report of a case. Oral Surg Oral Med Oral Pathol. 1985;60(5):482-484 Kraut RA. Bilateral coronoid hyperplasia: report of two cases. J Oral Maxillofac
f
[62]
[63]
oo
Surg. 1985;43(8):612-614
Praal FR. Limitation of mandibular movement due to bilateral mandibular coronoid
Tucker MR, Guilford WB, Howard CW. Coronoid process hyperplasia causing
e-
[64]
pr
process enlargement. J Oral Maxillofac Surg. 1984;42(8):534-536
restricted opening and facial asymmetry. Oral Surg Oral Med Oral Pathol. 1984;58(2):130-
[65]
Pr
132
Bernstein L, Fernandez B. Bilateral hyperplasia of the coronoid process of the
York BV, Cockerham S. Bilateral hyperplasia of the coronoid processes in siblings.
rn
[66]
al
mandible. Report of a case. Arch Otolaryngol. 1984;110(7):480-482
Oral Surg Oral Med Oral Pathol. 1983;56(6):584-585 Marra LM. Bilateral coronoid hyperplasia, a developmental defect. Oral Surg Oral
Jo u
[67]
Med Oral Pathol. 1983;55(1):10-13 [68]
Lucaya J, Herrera M, Vera J. Unilateral hyperplasia of the coronoid process in a
child: a cause of restricted opening of the mouth. Radiology. 1982;144(3):528 [69]
Javid B. Unilateral hyperplasia of the coronoid process of the mandible. Case
report. Int J Oral Surg. 1981;10(2):145-147
Page 18 of 36
[70]
Duffy BL. Case report--bilateral mandibular coronoid process hyperplasia. Anaesth
Intensive Care. 1980;8(4):484-486 [71]
Hecker R, Corwin JO. Bilateral coronoid hyperplasia: review of the literature and
report of case. J Oral Surg. 1980;38(8):606-608 [72]
Shuken RA, Girard KR. Bilateral mandibular coronoid hyperplasia. J Oral Surg.
Rivas PH. Reduction of mouth opening due to mandibular coronoid progess
oo
[73]
f
1979;37(10):744-746
enlargement. Report of a case. Oral Surg Oral Med Oral Pathol. 1979;47(2):131-134 Monks FT. Bilateral hyperplasia of the mandibular coronoid processes: a case
[75]
e-
report. Br J Oral Surg. 1978;16(1):31-37
pr
[74]
Michel RG, Hudson WR, Drawbaugh EJ, Baylin GJ. Exostosis of the mandibular
[76]
Pr
coronoid process. Ann Otol Rhinol Laryngol. 1977;86:12-16 Kallioniemi H, Oksala E, Lauttamus A. Unilateral hyperplasia of the mandibular
Shurman J. Bilateral hypertrophy of the coronoid processes. Anesthesiology.
rn
[77]
al
coronoid process. Case report. Proc Finn Dent Soc. 1975;71(5):184-190
1975;42(4):491-492
Scott AS, Frew AL, Jr. Bilateral enlargement of the mandibular coronoid processes
Jo u
[78]
in a patient with rheumatoid arthritis of the temporomandibular joints. J Oral Surg. 1975;33(10):787-789 [79]
Rusconi L, Brusati R. Restricted opening of the mouth from symmetrical bilateral
hyperplasia of the coronoid processes. J Oral Surg. 1974;32(6):452-456 [80]
van Hoof RF, Besling WFJ. Coronoid process enlargement. Br J Oral Surg
1973;10:339-348
Page 19 of 36
[81]
Bramley PA, Norman JE. Secondary enlargement of the mandibular coronoid
process. Br J Surg. 1972;59(6):426-429 [82]
Muldoon CJ. Bilateral coronoid hyperplasia. J Ir Dent Assoc. 1971;17(4):121-124
[83]
Hurd GK. Diagnosis and surgical management of coronoid process hyperplasia:
report of case. J Can Dent Assoc (Tor). 1970;36(10):373-375 Fitzpatrick BN. Bilateral hyperplasia of the mandibular coronoid process. Oral Surg
f
[84]
[85]
Nickerson JW, Jr., Grafft NL, Sazima HJ. Bilateral coronoid process enlargement:
pr
report of case. J Oral Surg. 1969;27(11):885-890
Allison ML, Wallace WR, Von Wyl H. Coronoid abnormalities causing limitation
e-
[86]
oo
Oral Med Oral Pathol. 1970;29(2):184-190
of mandibular movement. J Oral Surg. 1969;27(3):229-233
Pr
[87]Rowe NL. Bilateral Developmental Hyperplasia of the Mandibular Coronoid Process. A
Report of Two Cases. Br J Oral Surg. 1963;1:90-104 Hecht F, Beals. Inability to open mouth fully: an autosomal dominant phenotype
al
[88]
[89]
rn
with facultative campylodactyly and short stature. Birth Defects 1969;5:69-98 Veugelers M, Bressan M, McDermott DA et al. Mutation of perinatal myosin heavy
Jo u
chain associated with a Carney complex variant. N Eng J Med 2004;351:460-469 [90]
Leonardi R, Caltabiano M, Lo Muzio L, Gorlin RJ, Bucci P, Pannone G, Canfora
M, Sorge G. Bilateral hyperplasia of the mandibular coronoid process in patients with nevoid basal cell carcinoma syndrome: an undescribed sign. Am J Med Genet 2002; 110(4):400-403
Page 20 of 36
[91]
Mioche L, Bourdiol P, Martin JF, Noel Y. Variations in human masseter and
temporalis muscle activity related to food texture during free and side-imposed mastication. Arch Oral Biol 199;44:1005-1012 [92]
Armijo-Olivo S, Magee DJ. Electromyographic activity of the masticatory and
cervical muscles during resisted jaw opening movement. J Oral Rehabil 2007;34:184-194 Chakranarayan A, Jeyaraj P. Coronoid hyperplasia in chronic progressive trismus.
f
[93]
[94]
oo
Med Hypotheses 2011;77:863-868
Farrar WB, McCarty WL Jr. Inferior joint space arthrography and characteristics
Isberg A, Isacsson G, Nah KS. Mandibular coronoid process locking: a prospective
e-
[95]
pr
of condylar paths in internal derangements of the TMJ. J Prosthet Dent 1979;41:548-555
study of frequency and association with internal derangement of the temporomandibular
[96]
Pr
joint. Oral Surg Oral Med Oral Pathol 1987;63:275-279 Wenghoefer M, Martini M, Allam JP, Novak N, Reich R, Berge SJ. Hyperplasia of
al
the coronoid process in patients with ankylosing spondylitis (Bechterew disease). J
[97]
rn
Craniofac Surg 2008;19:1114-1118
Sarnat BG, Engel MB. A serial study of mandibular growth after removal of the
Jo u
condyle in the Macaca rhesus monkey. Plast Reconstr Surg 1951;7:364-380 [98]
Jamal BT, Taub D, Gold L. Contralateral coronoid hyperplasia in patients
undergoing hemimandibulectomy with disarticulation: a case series. J Oral Maxillofac Surg 2009;67(9):1821-1825 [99]
Puche M, Guijarro-Martínez R, Pérez-Herrezuelo G, Miragall L, Iglesias ME,
Martínez-Costa C. The hypothetical role of congenital hypotonia in the development of early coronoid hyperplasia. J Craniomaxillofac Surg 2012;40:e155-e158
Page 21 of 36
[100]
Chen CM, Chen CM, Ho CM, Huang IY. Gap coronoidotomy for management of
coronoid process hyperplasia of the mandible. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;112:e1-e4 [101]
Kubota Y, Takenoshita Y, Takamori K, Kanamoto M, Shirasuna K. Levandoski
panographic analysis in the diagnosis of hyperplasia of the coronoid process. Br J Oral
Stopa Z, Wanyura H, Kowalczyk P. Coronoid-condylar index in assessing of
oo
[102]
f
Maxillofac Surg 1999;37:409-411
pr
mandibular coronoid hyperplasia. Adv Med Sci 2013;58(2):429-433 LIST OF TABLES
Jo u
rn
al
Pr
e-
Table 1: Summary of case reports & case series included in this review
Page 22 of 36
Table 1: Summary of case reports & case series included in this review Authors/
Gend
Ons
Treatm
Typ
Associat
Treat
Surgic
Pre
Intr
Foll
Follo
Year
er
et
ent age
es
ed
ment
al
-op
a-
ow
w up
Age
(years)
approa
MO
op
up
perio
ch
(m
M
MO
d
m)
O
(m
(mont
(m
m)
hs)
history
(yea
oo
f
rs)
Schneble et
Ectom Male
NA
4
Bi
No
15
25
15
60
NA
NA
NA
NA
NA
IO
21
NA
NA
NA
IO
NA
NA
NA
12
IO
22
42
32
3
y
Fema et al/ 2018
NA
14
NA
30
Uni
[8] Ghazizadeh
Bi
Ribeiro da
15
Jo u
Male
rn
[9]
43
NA
Ectom
No
y
al
Male
No
Pr
le
e-
Tolentino
Silva et al/
NA
pr
al/ 2019 [7]
et al/2017
m)
Ectom Bi
NA y
2017 [10] Starch-
Jensen &
Male
Kjellerup/
NA
Ectom 18
Bi
No y
2017 [11]
Page 23 of 36
Romano et Ectom al/ 2017
Male
NA
37
Bi
No
IO
16
39
39
12
IO
20
38
40
12
13
41
39
12
EO
19
47
45
12
EO
13
38
43
12
EO
17
39
40
12
IO
15
NA
33
3
NA
NA
NA
NA
NA
y [12] Romano et Ectom al/ 2017
Male
NA
25
Bi
No y
[12] Romano et NA
43
Bi
No
IO
oo
Male
f
Ectom al/ 2017
y
Romano et
pr
[12]
Ectom
al/ 2017
Male
NA
27
Bi
No
e-
y
Romano et al/ 2017
Male
NA
29
Male
NA
Jo u
[12]
rn
Romano et al/ 2017
Bi
23
Bi
Ectom
No
al
[12]
Pr
[12]
y
Ectom No y
Acharya et al/ 2017 [13]
Male
13
Ectom 15.75
Bi
No y
Punyani & Fema Jasuja/
Ear 11
le
23
Uni
NA infection
2017 [14]
Page 24 of 36
Khandavilli Fema et al/ 2016
NA
16
Bi
NA
No Sx
No Sx
14
NA
NA
NA
NA
16
Bi
NA
No Sx
No Sx
10
NA
NA
NA
NA
0.25
Bi
No
le [15] Khandavilli Fema et al/ 2016 le [15] Monevska Ectom
f
Fema
IO
le
2
21
21
12
EO
5
10
NA
24
IO
20
41
41
12
No Sx
25
NA
NA
NA
IO
28
43
63
15
IO
32
35
65
18
IO
12
No
54
15
No Sx
15
NA
NA
NA
oo
et al/2016
y
[16] Pseudoca
pr
Balkin et
Ectom
al/ 2015
Male
0.59
2.17
Bi
mp
e-
y
todactyly
Choi et al/ Male
NA
31
2014 [18] Kim et al/ 13
Male
NA
Jo u
2014 [19]
rn
Kim et al/
43
Bi
21
No
Uni
No
15
y
No Sx
Ectom y
Kim et al/
Male
Ectom
No
Bi
al
Male 2014 [19]
Pr
[17]
Ectom 19
Bi
No
2014 [19]
y
Kim et al/
Ectom
Male
17.5
18
Uni
No
2014 [19]
y
Utsman et al/ 2013
Male
11
12
Bi
No
No Sx
[20]
Page 25 of 36
Sleeman et Fema al/ 2012
Ectom NA
7
Uni
Trauma
30 IO
le
15
y
NA
NA
3
[21] Newasker Ectom et al/ 2012
Male
NA
15
Uni
NA
EO
NA
NA
NA
6
Comb
23
NA
38
NA
21
30
NA
NA
20
NA
40
5
29
31
1
y [22] Ectom Male
NA
21
Uni
Trauma y
oo
2012 [23]
f
Bayar et al/
Robiony et
IO
Ectom Male
NA
NA
Bi
NA
(Endo
pr
al/ 2012
y
scope)
Costa et al/
Ectom
Male
NA
18
Bi
No
Pr
2012 [25] RamalhoFerreira et 23
Bi
2011[26]
Jo u
Peacock et Male
6
7
NA
y
Ectom
No
18. IO
y
rn
al/
26
al
Male
al/
e-
[24]
5
Ectom Uni
No
EO
16
40
38
6
EO
5
NA
35
18
NA
10
NA
28
NA
y
2011[27]
Galiѐ et al/
Fema
2010 [28]
le
NA
TMJ 3
Ectom
Uni arthrosis
y
Vaidhyanat Fema h & Raj/
Ectom NA
le
52
Bi
NA y
2010 [29]
Page 26 of 36
Iqbal et al/
Ectom Male
5
13
Uni
Trauma
2009 [30]
IO
30
NA
35
24
IO
30
50
43
15
IO
8
40
31
9
13
NA
40
12
IO
20
30
38
12
y
Yura et al/ Male
15
28
Uni
No
Otomy
2009 [31] Zhong et Fema al/ 2009
Ectom 26
39
Bi
No
le
y
f
[32]
oo
Fernández-
Ectom Ferro et al/
Male
NA
28
Bi
No
IO
y
pr
2008 [33] Gibbons & Abulhoul/
Male
16
36
Bi
e-
Ectom
NA
2007 [34] Mazzetto & Male
NA
Leovic et Male
17
Jo u
al/ 2006
rn
[35]
[36]
55
Bi
NA
No Sx
No Sx
32
NA
NA
NA
al
Hotta/ 2007
Pr
y
35
Bi
NA
Otomy
IO
15
NA
35
NA
Kursoglu & Capa/ 2006
Male
NA
24
Bi
No
No Sx
No Sx
27
NA
NA
NA
Male
NA
17
Bi
NA
No Sx
No Sx
14
NA
NA
NA
[37] Kursoglu & Capa/ 2006 [37]
Page 27 of 36
Satoh et al/
Ectom Male
12
13
Bi
No
2006 [38]
IO
27
40
45
8
IO
27
NA
6
42
IO
17
NA
40
72
y
Bertacci et al/ 2005
Male
15
25
Bi
No
Male
5
8
Bi
No
Otomy
[39] Mano et al/
Ectom y
f
2005 [40]
oo
Tieghi et
Ectom al/ 2005
Male
13
15
Bi
Trauma
IO
25
40
46
3
IO
25
40
40
20
IO
6
33
30
8
IO
21
NA
NA
18
IO
22
35
22
30
y
pr
[41] Tieghi et al/ 2005
Ectom
NA
17
Bi
le
e-
Fema
No
y
Pr
[41]
Abnorma
Fabie et al/
Fema le
Jo u
2002 [42]
8
swallowi
Ectom
Bi
rn
3
al
l
ng and
y
sucking reflex
Colquhoun et al/ 2002
Male
29
Ectom 32
Bi
No y
[43] Colquhoun Ectom et al/ 2002
Male
23
26
Bi
No y
[43]
Page 28 of 36
Gibbons et Ectom al/
Male
16
28
Bi
NA
EO
15
40
NA
NA
NA
25
NA
NA
NA
4
25
NA
NA
y 2001[44] Leonardi et al/
Male
NA
13
Bi
NBCCS
NA
2001[45] Moebius NA
1.5
Bi
syndrom
1999 [46]
f
Ectom Male
IO
8
oo
Turk et al/
NA
y e
pr
Moebius Turk et al/
Ectom
NA
NA
NA
Bi
IO
3010
y
40
e-
1999 [46]
syndrom
Loh et al/ Male
12
14
1997 [47] Loh et al/ NA
Loh et al/ Male
18
Jo u
1997 [47]
rn
1997 [47]
Loh et al/
Bi
22
Ectom
No
IO
13
22
32
12
IO
15
25
NA
NA
EO
5
20
NA
NA
IO
16
30
NA
NA
y Ectom
No y Ectom
Bi
No y
Fema
15
1997 [47]
41
Bi
al
Male
Pr
e
Ectom 25
Bi
No
le
y
Gerbino et
Male
14
15
Uni
No
Otomy
IO
15
NA
12
41
Male
15
32
Bi
NA
Otomy
IO
20
NA
60
42
al/ 1997 [5] Gerbino et al/ 1997 [5]
Page 29 of 36
Gerbino et Male
12
14
Uni
NA
Otomy
IO
12
NA
60
46
Male
10
13
Bi
NA
Otomy
IO
18
NA
15
40
Male
14
16
Bi
NA
Otomy
IO
20
NA
60
38
Male
30
40
Bi
No
IO
25
37
NA
NA
19
35
NA
NA
Comb
4
50
11
96
IO
21
NA
NA
NA
IO
23
38
32
14
IO
17
45
52
10
al/ 1997 [5] Gerbino et al/ 1997 [5] Gerbino et al/ 1997 [5] Ectom y
oo
1995 [48]
f
Currie et al/
Gibbons/
Ectom Male
17
34
Bi
No
IO
y
pr
1995 [49] Smyth & Wake/
Male
8
15
Bi
e-
Ectom
NA
1994 [50] Hönig et al/ Male
17
22
Uni
Fukumori
[52]
Male
14
23
Ectom
No
y
Short stature, Ectom
Bi
blepharo y
Jo u
et al/ 1993
rn
al
1994 [51]
Pr
y
chlasis
Totsuka & Fukuda/
Male
14
Ectom 17
Bi
No y
1991[53]
Page 30 of 36
Totsuka & Ectom Fukuda/
Male
10
13
Bi
No
IO
29
48
45
3
EO
22
NA
40
12
y 1991[53] Hayter & Ectom Robertson/
Male
15
16
Bi
No y
1989 [54] Shultz & 14
16
Bi
No
IO
20
40
48
24
IO
10
34
38
12
Comb
9
35
37
24
IO
14
45
37
3
oo
Male
f
Ectom Theisen/
y
Hall et
pr
1989 [55]
Ectom
al/1989
Male
12
23
Bi
No
e-
y
Hall et al/1989
Male
21
24
Macleod/ 1987 [57] Macleod/
14
Bi
Ectom
No
y
Ectom No y
NA
15
Bi
No
No Sx
No Sx
18
NA
NA
NA
Male
NA
17
Bi
No
No Sx
No Sx
20
NA
NA
NA
Male
NA
66
Bi
Trauma
IO
9
41
26
3
IO
38
60
45
3
Jo u
Male
NA
rn
Male
Bi
al
[56]
Pr
[56]
1987 [57] Macleod/
1987 [57] Macleod/
Ectom
1987 [57]
y
Macleod/
Ectom Male
1987 [57]
NA
47
Uni
Trauma y
Page 31 of 36
Giacomuzz
Arm Male
11
19
Bi
i/ 1986 [58]
No Sx
No Sx
11
NA
NA
NA
exostosis
Bronstein & Osborne/
Male
NA
20
Bi
Trauma
Otomy
IO
20
30
39
3
Male
NA
29
Bi
No
No Sx
No Sx
26
NA
NA
NA
44
54
Bi
No
1985 [59]
Gallimore/
f
Balcunas &
oo
1985 [60] Kreutz &
Ectom
le
le
17
18
No
Bi
14
Jo u
[64]
rn
Tucker et Male
45
24
IO
14
43
27
11
IO
15
NA
40
3
16
Uni
EO
22
40
44
3
IO
13
28
30
3
IO
10
NA
NA
NA
y
Ectom
No
al
[63]
Bi
Pr
38
Praal/1984
al/ 1984
50
Ectom
NA
Male
e-
Fema
1985 [62]
16
y
1985 [61] Kraut/
EO
pr
Fema Sanders/
y
Ectom No y
Bernstein &
Male
NA
Ectom 17
Bi
No
Fernandez/
y
1984 [65] York & Fema Cockerham
Ectom 6
le
7
Bi
No y
/ 1983 [66]
Page 32 of 36
York & Fema Cockerham
Ectom 11
12
Bi
No
le
IO
10
NA
NA
NA
IO
14
45
36
NA
NA
22
NA
NA
5
y
/ 1983 [66] Marra/
Ectom Male
NA
13
Bi
No
1983 [67]
y
Lucaya et Fema
Ectom 8.67
9
Uni
No
le
y
24.3 Male
1981[69]
Ectom 25
Uni
Trauma
3
Duffy et al/ 15
Bi
NA
41
3
IO
8
30
NA
NA
IO
16
48
NA
IO
12
35
28
3
Comb
9
30
40
8
IO
8
20
37
144
Male
14
16
Bi
Male
23
Jo u
1979 [72]
rn
Shuken &
Male
NA
38
Bi
Ectom y
Ectom 19
Uni
No y Difficult
Monks/
NA
y
No
1979 [73]
Male
Ectom
No
al
1980 [71]
Pr
y
Hecker &
Rivas/
No
e-
NA
1980 [70]
Girard/
11
Ectom
Male
Corwin/
IO
y
pr
Javid/
oo
[68]
f
al/ 1982
Ectom 50
Bi
extractio
1978 [74]
y n
Page 33 of 36
Michel et Fema al/ 1977
Ectom NA
30
Uni
No
le
IO
10
NA
NA
NA
IO
11
31
12
46
NA
22
NA
45
NA
y
[75] Kallioniemi Fema et al/ 1975
Ectom 15
20
Uni
No
le
y
[76] Ectom Male
NA
44
Bi
Trauma y
oo
1975 [77]
f
Shurman/
Scott &
Ectom Male
NA
25
Bi
No
EO
15
37
28
3
Otomy
IO
18
NA
38
7
No Sx
No Sx
13
NA
NA
NA
EO
9
NA
18
32
No Sx
17
NA
NA
NA
pr
Frew/ 1975
y
e-
[78] Mild
Brusati/
torticolli
Male
12
21
Bi
NA
Jo u
Male
rn
van Hoof & Besling/
s,
juvenile
al
1974 [79]
Pr
Rusconi &
diabetes
12
Bi
No
20
Bi
No
1973 [80]
van Hoof & Besling/
Male
NA
Ectom y
1973 [80] van Hoof & Besling/
Male
NA
46
Bi
No
No Sx
1973 [80]
Page 34 of 36
van Hoof & Ectom Besling/
Male
10
15
Bi
No
IO
24
42
6
42
IO
17
NA
NA
NA
y 1973 [80] van Hoof & Ectom Besling/
Male
NA
18
Uni
Trauma y
1973 [80] van Hoof & NA
18
Bi
No
NA
18
43
2
33
IO
17
35
NA
NA
Comb
10
NA
NA
NA
EO
11
35
6
35
IO
5
22
40
24
Comb
9
20
24
1
IO
14
45
NA
NA
oo
Male
f
Ectom Besling/
y
Bramley &
pr
1973 [80]
Ectom
Norman/
Male
19
24
Uni
No
e-
y
Muldoon/ Male
14
17
1971 [82]
Pr
1972 [81]
Bi
Ectom
Trauma
y
Male
13
Fitzpatrick/
18
Jo u
Male
22
rn
[83]
al
Right
Hurd/ 1970
27
Uni
Ectom TMJ y clicking Ectom
Bi
No
1970 [84]
y
Nickerson
et al/ 1969
Male
12
Ectom 22
Bi
No y
[85] Allison et Ectom al/ 1969
Male
15
18
Bi
No y
[86]
Page 35 of 36
Rowe/
Ectom Male
12
15
Bi
No
1963 [87]
IO
15
NA
35
14
No Sx
10
NA
NA
NA
y
Rowe/ Male
13
15
Bi
No
No Sx
1963 [87]
Jo u
rn
al
Pr
e-
pr
oo
f
Uni= Unilateral, Bi= Bilateral, Ectomy= Coronoidectomy, Otomy= Coronoidotomy, No Sx= No Surgery, IO= Intraoral, EO= Extraoral, Comb= Combined intraoral & extraoral, NA= not available
Page 36 of 36