Mandibular condylar hyperplasia (MCH) is a disorder of idiopathic origin in which pathological enlargement of the mandibular condyle is seen. Adams in 1836 was the first to describe the disorder, stating that it caused overdevelopment of the mandible and subsequent functional and aesthetic discomfort. Several case studies are found in the literature, and the rarity of the condition has been emphasized. This notion has, however, been challenged, and recent articles claim that the disorder is much more common in the population than most clinicians tend to believe.

Many theories have been presented; however, the pathological aetiology of the disorder remains unclear and is probably multifactorial. Some researchers have supported the ‘local circulatory theory’, which claims that the abnormal growth of the condyle is caused by an increased number of capillaries in the posterior superior anatomy of the condyles. Others have suggested that previous trauma, inflammation/infection of the temporomandibular joint (TMJ)/middle ear, osteomyelitis, osteochondromas, or chondromas may be initiating factors for MCH. Some authors suggest a hereditary, hormonal, or genetic influence, and TMJ loading has also been mentioned as a possible cause of MCH. Wolford and LeBanc have suggested that insufficient bone plate closure when cartilage from the proliferative layer is replaced by bone around age 20 years, e.g., as also seen in chondromas, osteochondromas, etc., could be a possible cause.

Another challenge is the lack of agreement in classification. In 1986, Obwegeser and Makek presented a classification system in which the disorder is separated into three categories: hemimandibular elongation (HE), with a horizontal growth vector; hemimandibular hyperplasia (HH), with a vertical growth vector; and a mixed form (HH + HE) that includes both pathological conditions. Typical clinical findings in HE are chin deviation towards the contralateral side and mandibular midline deviation towards the unaffected side. Clinical findings in HH are characterized as a compensatory overdevelopment of the maxilla on the affected side or an ipsilateral open bite with an occlusal cant. More recently, Wolford et al. suggested a simpler classification system in which condylar hyperactivity is suggested to be a pathological condition that causes overdevelopment of the condylar neck or head of the mandible, divided into two types: CH1 and CH2. This hyperactivity may be caused by various pathological conditions with different effects on the development of the facial skeleton. CH1 is caused by an accelerated growth of the normal growth mechanism, with a horizontal growth vector, and is divided into two entities: 1A, comprising bilateral abnormal growth of the mandibular condyles that is more or less symmetrical, and 1B, comprising unilateral, asymmetric abnormal condylar growth in which one side is more affected than the other, leaving an obvious asymmetrical condyle ( Fig. 1 ).

The classification system of Wolford et al.

Furthermore, Wolford et al. stated that 1A is the more common condition and that 1B is rarer but causes a distinct facial asymmetry. Both of these types present at an early age (from childhood and to the mid-20s) and are mostly self-limited. CH2 is caused by an accelerated growth of the normal growth mechanism, with a vertical growth vector. The aetiology for this is unknown. CH2 is claimed to present at any age and is not self-limited. The differential diagnosis of CH2 includes osteochondromas, osteomas, benign tumours, hemifacial hypertrophy, etc. When these pathologies are present, a somewhat similar clinical appearance to CH2 is seen; however, the distinct difference is that the accelerated motion has an aetiology and therefore cannot be called CH2.

Figure 2 illustrates the comparison between the Obwegeser and Makek and Wolford classification systems. In this study the focus was placed mainly on cases where condylar hyperplasia is caused by an accelerated growth of the normal growth mechanism in the condyle due to an unknown pathology.

Summary of the similarities between the classification systems of Wolford et al. (CH1A/B, CH2) and Obwegeser and Makek (HE, HH).

Today, no gold standard exists regarding the diagnosis of MCH. In addition, there is no agreement in the literature on the histopathology of MCH, and thus one cannot simply rely on a histopathological analysis of the hyperactive condyles to make the diagnosis of MCH. Prior attempts to classify the disorder histologically have been undertaken by Norman and Painter, Eslami et al., and Slootweg and Müller. Norman and Painter used histopathological findings based on 99m technetium (99mTc) scintigraphy to make an instrumental diagnosis of MCH. This was used to define the activity level of MCH. However, as later stated by Hodder et al., this qualitative method is sometimes inconsistent because the method is non-specific and hence not accurate enough to distinguish between active hyperplasia and other normally occurring active growth centres. Hodder et al. suggested that single photon emission computed tomography (SPECT) is more reliable because it has the ability to, more specifically, show condylar hyperactivity in a quantitative and accurate fashion. Several uptake values have been suggested, and a difference in uptake of 45% to 55% or more between the condyles is said to be an indication of unilateral condylar hyperplasia (UCH).

Wolford et al. have suggested that it is not necessary to use bone SPECT to show hyperactivity, and that hyperactivity can be shown by lateral cephalograms and clinical diagnostic techniques with serial assessments (6- to 12-month intervals). Additionally, it is suggested that bone scans are unnecessary or provide little information in bilateral cases. Additional diagnostic methods are clinical photographs, cast models in articulators, and conventional (CT) or cone beam computed tomography (CBCT) scans.

In the literature, the use of a high condylectomy in the treatment of MCH is controversial. The most important factor with MCH, and especially UCH, is that the disorder has a dynamic component and that a delayed intervention is possible after growth has ceased. However, this approach can be problematic because the development of asymmetry is very unpredictable and repair may thus be made more difficult. It is therefore relevant to discuss the effect of high condylectomy on patients with MCH because this surgical approach is designed to address the specific problem of the abnormal activity of the growth centre in the mandibular condyle.

The aim of this study was to undertake a comprehensive and systematic analysis of the current literature on the efficacy of high condylectomy in patients with MCH, and if possible to perform a meta-analysis of the results.

Materials and methods

In this systematic review, an attempt was made to identify the relevant literature concerning the effect of high condylectomy on both dental function and aesthetics in patients with UCH; the PRISMA statement was followed.

A systematic database search was performed using the National Center for Biotechnology Information to search MEDLINE (PubMed) and Embase. The search included articles published between 1994 and 2014 and included only articles in English and German, and was deliberately made wide to ensure that all relevant articles published on the subject could be identified.

The following two groups were compiled for the search using the following medical subject heading (MeSH) terms: group 1, “condylar hyperplasia” OR “facial asymmetry” OR facial asymmetry [mesh] OR “abnormal mandibular growth” OR “hemimandibular hyperplasia” OR “unilateral condylar hyperplasia” OR “hemimandibular elongation” OR “early high condylar hyperplasia” OR “chin deviation” OR “hemifacial hypertrophy” OR unilateral micrognathia OR laterognathia OR “hemimandibular hyperplasia”; and group 2, treatment outcome OR “mandibular high condylectomy” OR “high condylectomy” OR efficacy OR “efficacy of high condylectomy”. An additional hand search of the bibliographies of the articles that met the inclusion criteria was performed.

The screening was carried out using the following inclusion and exclusion criteria. Inclusion criteria: a relevant sample size of at least five patients to avoid singular case studies, a relevant background history of the patient to ensure that condylar hyperplasia was not of any other aetiology, an informative clinical description of the tools used to diagnose the condylar hyperplasia patient, and a thorough follow-up procedure with information that included the level of discomfort. Exclusion criteria: case reports with fewer than five patients, differential diagnoses causing facial asymmetry (including hemifacial microsomia, trauma to the mandibular condylar growth centre, and benign or malignant condyle tumours), no description of the diagnostic setup and follow-up, and cases in which the MCH was managed with procedures other than a high condylectomy or condylectomy.

The titles of articles were first screened for relevancy according to the inclusion criteria. If these were met, the abstracts were screened according to the inclusion and exclusion criteria. If the abstract did not give sufficient information, the full-text article was retrieved (see Fig. 3 ).

Systematic search of the literature.

The following data were retrieved from the relevant articles and entered into an excel spreadsheet: author, year of publication, how the MCH was classified, the affected side and activity of the MCH, sample size, sex, age, aetiology, diagnostic methods, procedure and level of excised bone in the high condylectomy, surgical procedures performed in addition to the high condylectomy, patient discomfort, nerve damage, and the result after the high condylectomy was performed. The data are presented in Table 1 . The Cochrane Collaboration tool for the assessment of the risk of bias was used to evaluate selection, performance, detection, attrition, and reporting risk of bias.

Table 1

Summary of the 11 articles meeting the inclusion criteria.

Author, year	Classification type	Affected side Type	Number of patients	Sex F/M	Age range (mean)
Chiarini et al., 2014	Wolford	5 L 5 CH2	5	2 F/3 M	14–17 (16.8) years
Jones and Tier, 2012	Obwegeser and Makek, Wolford	Unknown 13 CH1B, 3 CH2, and 1 CH2 due to osteochondroma	17	15 F/2 M	Unknown
Villanueva-Alcojol et al., 2011	Obwegeser and Makek	22 R and 14 L 24 HH, 8 HE, 4 HH + HE	36	25 F/11 M	11–42 (22.7) years
Saridin et al., 2010	Unknown	16 R, 16 L, 1 bilateral Unknown	33/46 agreed to participate (31 subjects who were age- and gender-matched to the patient cohort served as a control group and entered the same research protocol)	18 F/15 M	19–48 (26.7) years
Brusati et al., 2010	Obwegeser and Makek, Wolford	Unknown	15	Unknown	12–42 (22) years
Wolford et al., 2009	Wolford	Unknown 36 CH1A, 18 CH1B	42/54 High condylectomy, disc repositioning, and orthognathic surgery 12/54 Orthognathic surgery only	36 F/18 M	13–24 (16.6) years
Deleurant et al., 2008	Obwegeser and Makek	Equally affected 7 HE	7/47 met criteria	6 F/1 M	13–25 (16.3) years
Lippold et al., 2007	Obwegeser and Makek	4 L, 2 R 6 HH	6	3 F/3 M	22–30 (27) years
Wolford et al., 2002	Wolford	Unknown 24 CH1A, 13 CH1B	25/37 High condylectomy and orthognathic surgery 12/37 Orthognathic surgery only	20 F/17 M	13–25 (16.7) years
Appel et al., 1997	Obwegeser and Makek	Unknown 6 HE, 7 HH, 3 HE + HH, 1 deformed condyle	17	Unknown	10–36 (22.5) years
Chen et al., 1996	Obwegeser and Makek	6 R and 3 L 6 HH, 3 HE + HH	9	7 F/2 M	18–58 (28.2) years
Author, year	Orthodontic treatment	History (family history, prior trauma)	Prior symptoms	Clinical examination	Clinical photos/study models
Chiarini et al., 2014	Yes, preop.	Unknown	Unknown	Mild facial asymmetry, canting of the occlusal plane, active laterognathia, no lateral hyperplastic mandibular lower border	Yes/yes
Jones and Tier, 2012	Yes, preop./postop.	Unknown	Unknown	Yes, no description	Yes/yes
Villanueva-Alcojol et al., 2011	Yes, postop.	No neoplasia/dysplasia	13 patients had TMJ mild pain/clicking	Occlusal disturbance and/or chin deviation towards the opposite side	Yes/yes
Saridin et al., 2010	Unknown	Unknown	Unknown	Made according to the RDC/TMD	Yes/yes
Brusati et al., 2010	Yes, preop.	Unknown	Unknown	Yes, no detail	Yes/yes
Wolford et al., 2009	Unknown	Unknown	No TMJ pain, no jaw dysfunction, no dietary dysfunction	MIO and lateral excursion	Yes/yes
Deleurant et al., 2008	Yes, preop.	Unknown	Unknown	Unknown	Yes/yes
Lippold et al., 2007	Yes, 5 patients preop. and postop. finishing 6 weeks after	Unknown	2 patients moderate, 3 patients mild, 1 patient no TMJ dysfunction according to Helkimo index	TMJ evaluation according to Helkimo index/electronic digital sliding calliper measurement on inter-incisal opening/chin deviation, tilting of occlusal plane	Yes/yes
Wolford et al., 2002	Yes, preop.	Approx. a third of bilateral cases had a family history	Mean TMJ 0.6; mean jaw function 3.6; mean diet 0.7	MIO and lateral excursion	Yes/yes
Appel et al., 1997	Unknown	Unknown	Symptoms started 2 years prior: pain, swelling, movement problems, but not that severe	Unknown	Yes/yes
Chen et al., 1996	Yes, postop.	No prior trauma	No TMJ complaints, no orofacial pain with opening	Unilateral enlargement of the mandibular condyle (with down bowing), condylar neck, ramus, and mandibular body; chin deviation to the unaffected side	Yes/yes
Author, year	Radiological examination	SPECT bone scintigraphy a	Bone excised	Histopathological examination	TMJ symptoms
Chiarini et al., 2014	CT/cephalograms	Yes, 99mTc	6 mm	None	None (mean VAS 2.4)
Jones and Tier, 2012	Lateral/posterior/anterior cephalometric projections	Yes, 99mTc	6 mm	None	Unknown
Villanueva-Alcojol et al., 2011	Pantomograms/postero-anterior and lateral cephalograms	Yes, 99mTc	4–5 mm	18/36 classified by Slootweg and Müller	None, not detailed
Saridin et al., 2010	Yes, no details	Yes, 99mTc	≥5 mm	None	GCP = 0 for 22/33, GCP = 1 for 6/33, GCP = 2 for 2/33; 3/33 excluded due to inconsistent data in the questionnaire
Brusati et al., 2010	Pantomograms/postero-anterior and lateral cephalograms	Yes, 99mTc	5–7 mm	None	8 patients had excellent articular function both objectively and subjectively; 6 patients had additional deviation in opening, lateral excursion reduced on the affected side; 1 patient had deviation in mouth opening, lower lateral excursion
Wolford et al., 2009	Lateral cephalometric projections	None	3–5 mm	None	Little improvement
Deleurant et al., 2008	Pantomograms	Yes, 99mTc	2–3 mm	None	Maximum mouth opening reduced by 50% after HC; regained 20% with OS, achieving in total about 70% of the initial mean value. In T6, 5 patients showed a gain of 83–95% and 2 patients plus 2% and plus 27%, respectively
Lippold et al., 2007	Pantomograms/frontal lateral cephalograms/CT	Yes, 99mTc	Unknown	According to Eslami et al.; affected condyle showed more signs similar to condylar arthrosis	3 patients improved in TMJ dysfunction postop. (Helkimo index)
Wolford et al., 2002	Lateral cephalometric projections	None	3–5 mm excised	None	Mean TMJ 0.3
Appel et al., 1997	Yes, unknown	Yes, 99mTc	1.5–3 mm excised	None	No symptoms
Chen et al., 1996	Pantomograms	6 patients 99mTc	Unknown	None	Unknown
Author, year	Pain	Results	Depression/nerve damage	Additional surgery
Chiarini et al., 2014	Swelling, trismus, and pain resolved within a month	Satisfactory TMJ function and stable occlusion	Unknown/none	None
Jones and Tier, 2012	Unknown	Satisfactory results where activity in condylar hyperplasia	Unknown	Orthognathic surgery in 17 patients, costochondral graft in 3 patients
Villanueva-Alcojol et al., 2011	Unknown	Satisfactory at 4.3 years follow-up	Unknown	6 patients (4 BSSO, 2 mentoplasties, 1 angle prostheses)
Saridin et al., 2010	3 patients myofascial pain; 0 patients myofascial pain with limited opening; 1 patient disc displacement without reduction with limited opening; 2 patients arthralgia symptoms; 1 patient osteoarthritis; 5 patients osteoarthrosis; 3 patients had more than one diagnosis	Satisfactory at 4.3 years follow-up	Not different from control group, therefore this can be disregarded	Unknown
Brusati et al., 2010	1 patient pain and noise	Satisfactory; when active condylar hyperplasia, should be considered especially in younger patients	Unknown	Recommended postsurgical physiotherapy and additional orthognathic surgery for aesthetic correction
Wolford et al., 2009	None	Satisfactory; only 1/42 grew back in class III, while all 12 patients in the control group with no HC had relapse	Unknown	Recommended TMJ articular disc is repositioned and stabilized to cover the articulating surface of the new condyle or defer correction until full growth and then only orthognathic surgery
Deleurant et al., 2008	Unknown	Satisfactory	Unknown	Recommended 1 year later BSSO and Le Fort I for optimal aesthetic results
Lippold et al., 2007	None	Satisfactory	Unknown	Recommended Le Fort I osteotomy in addition
Wolford et al., 2002	Mean jaw function 2.4/mean diet 0.5	Satisfactory; only 1/25 grew back in class III, while all 12 patients in the control group with no HC had relapse	Unknown	If an active condylar hyperplasia, then condylectomy (usually in younger patients); if inactive condylar hyperplasia, no condylectomy as orthognathic surgery is sufficient
Appel et al., 1997	No pain	Unsatisfactory	Unknown/1 patient, auriculotemporal nerve	7 patients underwent a second surgical intervention after 6–14 months; 3 patients are still planned for the procedure; 6 patients denied a second surgical intervention
Chen et al., 1996	Unknown	Satisfactory	Unknown	Additional surgery was performed to level out the occlusal plane

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