Int. J. Oral Maxillofac. Surg.

2016; 45: 60–71

http://dx.doi.org/10.1016/j.ijom.2015.09.002, available online at http://www.sciencedirect.com

Systematic Review
TMJ Disorders

High condylectomy for the S. Ghawsi, E. Aagaard,

T. H. Thygesen
Department of Oral and Maxillofacial Surgery,

treatment of mandibular Odense University Hospital, Odense,

Denmark

condylar hyperplasia: a
systematic review of the
literature
S. Ghawsi, E. Aagaard, T.H. Thygesen: High condylectomy for the treatment of
mandibular condylar hyperplasia: a systematic review of the literature. Int. J. Oral
Maxillofac. Surg. 2016; 45: 60–71. # 2015 International Association of Oral and
Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.

Abstract. Mandibular condylar hyperplasia (MCH) is a rare, idiopathic disorder,

which can cause both functional and aesthetic problems. MCH has often been
described in the literature, but a comprehensive analysis of the current literature on
MCH has not been undertaken. This study presents a systematic review analyzing
the efficacy of high condylectomy in patients with MCH, with an emphasis on its
role in the management of unilateral condylar hyperplasia. A systematic search of
the current literature on high condylectomy was performed to find studies with
sample sizes of more than five patients using a set of inclusion/exclusion criteria.
The search terms revealed 664 studies, of which only 11 articles with a total of 289
patients were eligible for inclusion. Due to differences in the presentation of data, a
Key words: mandibular condylar hyperplasia;
meta-analysis was not conducted. High condylectomy appears to be a relevant
unilateral condylar hyperplasia; high condylect-
surgical method to correct unilateral condylar hyperplasia. The current literature omy.
indicates large variations in terms of aetiology, use of diagnostic tools, and preferred
time of intervention. Thus, further systematic studies are needed to determine which Accepted for publication 4 September 2015
procedures offer the best aesthetic and functional results. Available online 19 September 2015

Mandibular condylar hyperplasia (MCH)
is a disorder of idiopathic origin in which
pathological enlargement of the mandibu-
lar 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.1 Several case studies are found
in the literature, and the rarity of the condi-
tion has been emphasized.2,3 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.4,5
Many theories have been presented;
however, the pathological aetiology of
the disorder remains unclear and is proba-
bly multifactorial. Some researchers have
supported the ‘local circulatory theory’,
which claims that the abnormal growth of
the condyle is caused by an increased

0901-5027/01060 + 012 # 2015 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.
 High condylectomy for the treatment of MCH 61

number of capillaries in the posterior
superior anatomy of the condyles.6 Others
have suggested that previous trauma,1,7–13
inflammation/infection of the temporo-
mandibular joint (TMJ)/middle ear,
osteomyelitis, osteochondromas, or chon-
dromas may be initiating factors for
MCH.7,14,15 Some authors suggest a
hereditary,2,16–18 hormonal, or genetic in-
fluence,19–21 and TMJ loading has also
been mentioned as a possible cause of
MCH.22,23 Wolford and LeBanc have sug-
gested 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.24
Another challenge is the lack of agree-
ment in classification. In 1986, Obwegeser
and Makek presented a classification sys-
tem in which the disorder is separated into
three categories: hemimandibular elonga-
tion (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.25 Typical clinical findings in
HE are chin deviation towards the contra-
lateral side and mandibular midline devi-
ation towards the unaffected side. Clinical
findings in HH are characterized as a
compensatory overdevelopment of the
maxilla on the affected side or an ipsilat-
eral open bite with an occlusal cant. More
recently, Wolford et al.4,5 suggested a
simpler classification system in which
condylar hyperactivity is suggested to be
a pathological condition that causes over-
development 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 vec-
tor, and is divided into two entities: 1A,
comprising bilateral abnormal growth of
the mandibular condyles that is more or
less symmetrical, and 1B, comprising uni-
lateral, asymmetric abnormal condylar
growth in which one side is more affected
than the other, leaving an obvious asym-
metrical condyle (Fig. 1).
Furthermore, Wolford et al. stated that
1A is the more common condition and that
1B is rarer but causes a distinct facial
asymmetry.4 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 osteochondro-
mas, osteomas, benign tumours, hemifa-
cial hypertrophy, etc. When these
pathologies are present, a somewhat simi-
lar 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 be-
tween the Obwegeser and Makek and
Wolford classification systems. In this
study the focus was placed mainly on

Clinical and radiographic characteriscs observed in paents with bilateral, symmetrical,

acve mandibular condylar hyperplasia type 1 according to the classificaon of Wolford et al.

1. Increased length of condylar head and neck, without a significant volumetric increase in the
size of the condylar head

2. Mandibular growth occurring at accelerated rate

3. Mandible connuing to grow beyond the normal growth years

4. Worsening class III skeletal and occlusal relaonship

5. Worsening aesthecs

6. Obtuse gonial angles

7. Decreased angulaon of lower incisors and increased angulaon of upper incisors

8. Decreased vercal height of the posterior mandibular body

9. High mandibular plane angle

10. Narrow anterior–posterior and mediolateral dimensions of the rami and symphysis in more
severe cases

Addional characteriscs in asymmetrical cases

1. TMJ arcular disc displacement and arthris on the contralateral side as a result of increased
loading of that joint caused by the condylar hyperplasia on the opposite side

2. Worsening facial occlusal asymmetry, with the mandible progressively shiing towards the
contralateral side

3. Unilateral posterior crossbite on the contralateral side

4. Transverse bowing of the mandibular body on the ipsilateral side

5. Transverse flaening of the mandibular body on the contralateral side

Fig. 1. The classification system of Wolford et al.

62 Ghawsi et al.
CH 1A: Bilateral, symmetrical, condylar hyperplasia (HE)
CH 1B: Unilateral, asymmetrical, condylar hyperplasia (HE)
CH 2: Unilateral, asymmetrical, condylar hyperplasia (HH)
Fig. 2. Summary of the similarities between the classification systems of Wolford et al. (CH1A/
B, CH2) and Obwegeser and Makek (HE, HH).
cases where condylar hyperplasia is
caused by an accelerated growth of the
normal growth mechanism in the condyle
due to an unknown pathology.26
Today, no gold standard exists regard-
ing the diagnosis of MCH. In addition,
there is no agreement in the literature on
the histopathology of MCH,27–29 and thus
one cannot simply rely on a histopatho-
logical analysis of the hyperactive con-
dyles to make the diagnosis of MCH. Prior
attempts to classify the disorder histologi-
cally have been undertaken by Norman
and Painter,3 Eslami et al.,30 and Slootweg
and Müller.22 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.31 Hodder et al. suggested
that single photon emission computed
tomography (SPECT) is more reliable be-
cause it has the ability to, more specifical-
ly, 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 hyperpla-
sia (UCH).32–34
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.5 Additional
diagnostic methods are clinical photo-
graphs, cast models in articulators, and
conventional (CT) or cone beam comput-
ed tomography (CBCT) scans.
In the literature, the use of a high con-
dylectomy 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 ap-
proach can be problematic because the
development of asymmetry is very unpre-
dictable 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.35,36
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.37
Materials and methods
In this systematic review, an attempt was
made to identify the relevant literature
concerning the effect of high condylect-
omy on both dental function and aesthetics
in patients with UCH; the PRISMA state-
ment was followed.37
A systematic database search was per-
formed using the National Center for Bio-
technology Information to search
MEDLINE (PubMed) and Embase. The
search included articles published be-
tween 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 com-
piled for the search using the following
medical subject heading (MeSH) terms:
group 1, ‘‘condylar hyperplasia’’ OR ‘‘fa-
cial asymmetry’’ OR facial asymmetry
[mesh] OR ‘‘abnormal mandibular
growth’’ OR ‘‘hemimandibular hyperpla-
sia’’ OR ‘‘unilateral condylar hyperplasia’’
OR ‘‘hemimandibular elongation’’ OR
‘‘early high condylar hyperplasia’’ OR
‘‘chin deviation’’ OR ‘‘hemifacial hyper-
trophy’’ OR unilateral micrognathia OR
laterognathia OR ‘‘hemimandibular hyper-
plasia’’; and group 2, treatment outcome
OR ‘‘mandibular high condylectomy’’ OR
‘‘high condylectomy’’ OR efficacy OR
‘‘efficacy of high condylectomy’’. An ad-
ditional 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 histo-
ry of the patient to ensure that condylar
hyperplasia was not of any other aetiol-
ogy, an informative clinical description of
the tools used to diagnose the condylar
hyperplasia patient, and a thorough fol-
low-up procedure with information that
included the level of discomfort. Exclu-
sion criteria: case reports with fewer than
five patients, differential diagnoses caus-
ing facial asymmetry (including hemifa-
cial microsomia, trauma to the mandibular
condylar growth centre, and benign or
malignant condyle tumours), no descrip-
tion of the diagnostic setup and follow-up,
and cases in which the MCH was managed
with procedures other than a high condy-
lectomy 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).
The following data were retrieved from
the relevant articles and entered into an
excel spreadsheet: author, year of publi-
cation, how the MCH was classified, the
affected side and activity of the MCH,
sample size, sex, age, aetiology, diagnos-
tic methods, procedure and level of ex-
cised bone in the high condylectomy,
surgical procedures performed in addition
to the high condylectomy, patient discom-
fort, nerve damage, and the result after
the high condylectomy was performed.
The data are presented in Table 1. The
Cochrane Collaboration tool for the as-
sessment of the risk of bias was used to
evaluate selection, performance, detec-
tion, attrition, and reporting risk of bias.38
Results
The search resulted in a total of 664
articles with at least one MeSH term in
both groups. Initially, titles were screened
for the inclusion criteria, and 605 articles
were excluded as they had no relevance to
the subject of high condylectomy in the
treatment of MCH. The abstracts of the
remaining 59 articles were reviewed, and
39 articles were excluded as most were
case studies and did not include the high
 High condylectomy for the treatment of MCH 63

293 Additional studies

664 records identified
identified through
through database searching
bibliographies

605 Excluded due to 113 Excluded due to

exclusion criteria exclusion criteria
664 headlines screened for 180 Titles screened for
eligibility eligibility after removal of
duplication

39 Excluded because 61 Excluded because

59 Abstracts assessed for 67 Abstracts assessed for
abstract did not meet abstract did not meet
eligibility eligibility
inclusion criteria inclusion criteria

20 Full-text articles 6 Full-text articles assessed

assessed for eligibility for eligibility
9 Full-text articles did not 6 Full-text articles did not
meet inclusion criteria meet inclusion criteria

Bibliography search
11 Articles met inclusion
revealed no additional
criteria
articles

11 Studies included in
qualitative synthesis

Fig. 3. Systematic search of the literature.

condylectomy procedure. The remaining
20 articles were reviewed in full-text, but
only 11 met the inclusion criteria4,5,39–47
(Fig. 3). An additional search of the bibli-
ographies of the included articles was
made, which created a database of 293
articles. The database was screened for
duplications, after which 180 articles
remained; 113 were excluded following
screening of the titles. A further 61 titles
were excluded as the abstract did not meet
the inclusion criteria. Six articles were
reviewed in full text. Following the appli-
cation of the inclusion and exclusion cri-
teria, this did not result in any further
addition to the list of articles; most of
the articles were either outdated or single
case studies (Fig. 3). The final 11 articles
were published between 1996 and 2014.
The number of patients in the articles
included ranged from 5 to 54, for a total of
289 patients. In one article, the mean age
was not given.44 From the remaining 10
articles, the mean age was 21.6 years
(standard deviation  4.42 years; range
10–58 years) for 272 patients.
Five of the articles used the classifica-
tion system of Obwegeser and Makek, two
articles used a combination of Obwegeser
and Makek and Wolford et al., three arti-
cles used only Wolford et al., and one
article used an unknown classification
system. Furthermore, an additional histo-
logical classification was made in two
articles, one according to Slootweg and
Müller22 and the other according to Eslami
et al.30 In only five of the articles was the
affected side mentioned: 42 of the cases of
MCH were on the left and 46 on the right.
Most researchers reported that the two
sides were affected equally. Some have
found the left side to be more affected,48
while others have found the right side to be
more affected.49,50 Thus there was close to
equal representation of the two affected
sides. In 10 of the articles, a combined
classification system was used based on
Obwegeser and Makek and/or Wolford
et al.: a total of 125 patients had
HE (CH1A + 1B), 51 patients had HH
(CH2), 10 patients had a mixed form
(HE + HH), and one patient was
excluded because CH2 was caused by
an osteochondroma.
In nine of the articles, the number of
male (n = 72) and female patients
(n = 132) affected by MCH was noted.
This revealed an approximate female to
male sex ratio of 11:6. MCH is usually
reported as being found equally in male
and female patients.51,52 However, a fe-
male predominance has been reported,
with female to male ratios of 25:11,47
7:2,19 and 3:1.53 It has also been suggested
that there is an association between female
gender and right-side MCH, whereas in
male patients, the left side is affected more
often. The data in this review did not
provide precise enough information to
make a comparison.
No detailed data were available that
outlined a suggested age for intervention;
however, six articles supported an early
intervention.4,5,40–42,47
All articles suggested the combined use
of clinical examinations (photographs,
cast models of dentition, radiology, scin-
tigraphy, SPECT, and a CT scan) to
diagnose MCH. One article used panoram-
ic X-ray as a diagnostic tool. This study,
however, emphasized that the panoramic
view provided insufficient information,
but that it was used due to the lack of
proper CT equipment.43 The reliability of
64 Ghawsi et al.

Table 1. Summary of the 11 articles meeting the inclusion criteria.

Classification Affected side Number of
Author, year type Type patients Sex F/M Age range (mean)
42
Chiarini et al., 2014 Wolford 5L 5 2 F/3 M 14–17 (16.8) years
5 CH2
44
Jones and Tier, 2012 Obwegeser and Unknown 17 15 F/2 M Unknown
Makek, Wolford 13 CH1B, 3 CH2,
and 1 CH2 due to
osteochondroma
Villanueva-Alcojol Obwegeser and 22 R and 14 L 36 25 F/11 M 11–42 (22.7) years
et al., 201147 Makek 24 HH, 8 HE, 4
HH + HE
Saridin et al., 201046 Unknown 16 R, 16 L, 1 33/46 agreed to 18 F/15 M 19–48 (26.7) years
bilateral participate (31
Unknown subjects who
were age- and
gender-matched
to the patient
cohort served as a
control group and
entered the same
research
protocol)
Brusati et al., 201040 Obwegeser and Unknown 15 Unknown 12–42 (22) years
Makek, Wolford
Wolford et al., 20095 Wolford Unknown 42/54 High 36 F/18 M 13–24 (16.6) years
36 CH1A, 18 CH1B condylectomy,
disc
repositioning,
and orthognathic
surgery
12/54
Orthognathic
surgery only
Deleurant et al., 200843 Obwegeser and Equally affected 7/47 met criteria 6 F/1 M 13–25 (16.3) years
Makek 7 HE
Lippold et al., 200745 Obwegeser and 4 L, 2 R 6 3 F/3 M 22–30 (27) years
Makek 6 HH
4
Wolford et al., 2002 Wolford Unknown 25/37 High 20 F/17 M 13–25 (16.7) years
24 CH1A, 13 CH1B condylectomy
and orthognathic
surgery
12/37
Orthognathic
surgery only
Appel et al., 199739 Obwegeser and Unknown 17 Unknown 10–36 (22.5) years
Makek 6 HE, 7 HH, 3
HE + HH, 1
deformed condyle
Chen et al., 199641 Obwegeser and 6 R and 3 L 9 7 F/2 M 18–58 (28.2) years
Makek 6 HH, 3 HE + HH
Author, year Orthodontic History (family Prior symptoms Clinical examination Clinical photos/
treatment history, prior study models
trauma)
Chiarini et al., 201442 Yes, preop. Unknown Unknown Mild facial asymmetry, Yes/yes
canting of the occlusal
plane, active
laterognathia, no lateral
hyperplastic
mandibular lower
border
Jones and Tier, 201244 Yes, preop./ Unknown Unknown Yes, no description Yes/yes
postop.
Villanueva-Alcojol Yes, postop. No neoplasia/ 13 patients had Occlusal disturbance Yes/yes
et al., 201147 dysplasia TMJ mild pain/ and/or chin deviation
clicking towards the opposite
side
Saridin et al., 201046 Unknown Unknown Unknown Made according to the Yes/yes
RDC/TMD
 High condylectomy for the treatment of MCH 65

Table 1 (Continued )
Classification Affected side Number of
Author, year type Type patients Sex F/M Age range (mean)
Brusati et al., 201040 Yes, preop. Unknown Unknown Yes, no detail Yes/yes
Wolford et al., 20095 Unknown Unknown No TMJ pain, no MIO and lateral Yes/yes
jaw dysfunction, excursion
no dietary
dysfunction
Deleurant et al., 200843 Yes, preop. Unknown Unknown Unknown Yes/yes
Lippold et al., 200745 Yes, 5 patients Unknown 2 patients TMJ evaluation Yes/yes
preop. and moderate, 3 according to Helkimo
postop. finishing patients mild, 1 index/electronic digital
6 weeks after patient no TMJ sliding calliper
dysfunction measurement on inter-
according to incisal opening/chin
Helkimo index deviation, tilting of
occlusal plane
Wolford et al., 20024 Yes, preop. Approx. a third of Mean TMJ 0.6; MIO and lateral Yes/yes
bilateral cases had a mean jaw excursion
family history function 3.6;
mean diet 0.7
Appel et al., 199739 Unknown Unknown Symptoms Unknown Yes/yes
started 2 years
prior: pain,
swelling,
movement
problems, but not
that severe
Chen et al., 199641 Yes, postop. No prior trauma No TMJ Unilateral enlargement Yes/yes
complaints, no of the mandibular
orofacial pain condyle (with down
with opening bowing), condylar
neck, ramus, and
mandibular body; chin
deviation to the
unaffected side
Author, year Radiological SPECT bone Bone excised Histopathological TMJ symptoms
examination scintigraphya examination
Chiarini et al., 201442 CT/ Yes, 99mTc 6 mm None None (mean VAS
cephalograms 2.4)
Jones and Tier, 201244 Lateral/posterior/ Yes, 99mTc 6 mm None Unknown
anterior
cephalometric
projections
Villanueva-Alcojol Pantomograms/ Yes, 99mTc 4–5 mm 18/36 classified by None, not detailed
et al., 201147 postero-anterior Slootweg and Müller
and lateral
cephalograms
Saridin et al., 201046 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., 201040 Pantomograms/ Yes, 99mTc 5–7 mm None 8 patients had
postero-anterior excellent articular
and lateral function both
cephalograms 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
66 Ghawsi et al.

Table 1 (Continued )
Classification Affected side Number of
Author, year type Type patients Sex F/M Age range (mean)
Wolford et al., 20095 Lateral None 3–5 mm None Little improvement
cephalometric
projections
Deleurant et al., 200843 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., 200745 Pantomograms/ Yes, 99mTc Unknown According to Eslami 3 patients improved
frontal lateral et al.; affected condyle in TMJ dysfunction
cephalograms/ showed more signs postop. (Helkimo
CT similar to condylar index)
arthrosis
Wolford et al., 20024 Lateral None 3–5 mm excised None Mean TMJ 0.3
cephalometric
projections
Appel et al., 199739 Yes, unknown Yes, 99mTc 1.5–3 mm None No symptoms
excised
Chen et al., 199641 Pantomograms 6 patients 99mTc Unknown None Unknown
Author, year Pain Results Depression/nerve Additional surgery
damage
Chiarini et al., 201442 Swelling, Satisfactory TMJ Unknown/none None
trismus, and pain function and stable
resolved within a occlusion
month
Jones and Tier, 201244 Unknown Satisfactory results Unknown Orthognathic surgery
where activity in in 17 patients,
condylar costochondral graft in 3
hyperplasia patients
Villanueva-Alcojol Unknown Satisfactory at 4.3 Unknown 6 patients (4 BSSO, 2
et al., 201147 years follow-up mentoplasties, 1 angle
prostheses)
Saridin et al., 201046 3 patients Satisfactory at 4.3 Not different Unknown
myofascial pain; years follow-up from control
0 patients group, therefore
myofascial pain this can be
with limited disregarded
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
Brusati et al., 201040 1 patient pain and Satisfactory; when Unknown Recommended
noise active condylar postsurgical
hyperplasia, should physiotherapy and
be considered additional orthognathic
especially in surgery for aesthetic
younger patients correction
 High condylectomy for the treatment of MCH 67

Table 1 (Continued )
Classification Affected side Number of
Author, year type Type patients Sex F/M Age range (mean)
Wolford et al., 20095 None Satisfactory; only 1/ Unknown Recommended TMJ
42 grew back in articular disc is
class III, while all 12 repositioned and
patients in the stabilized to cover the
control group with articulating surface of
no HC had relapse the new condyle or
defer correction until
full growth and then
only orthognathic
surgery
Deleurant et al., 200843 Unknown Satisfactory Unknown Recommended 1 year
later BSSO and Le Fort
I for optimal aesthetic
results
Lippold et al., 200745 None Satisfactory Unknown Recommended Le Fort
I osteotomy in addition
Wolford et al., 20024 Mean jaw Satisfactory; only 1/ Unknown If an active condylar
function 2.4/ 25 grew back in hyperplasia, then
mean diet 0.5 class III, while all 12 condylectomy (usually
patients in the in younger patients); if
control group with inactive condylar
no HC had relapse hyperplasia, no
condylectomy as
orthognathic surgery is
sufficient
Appel et al., 199739 No pain Unsatisfactory Unknown/1 7 patients underwent a
patient, second surgical
auriculotemporal intervention after 6–14
nerve months; 3 patients are
still planned for the
procedure; 6 patients
denied a second
surgical intervention
Chen et al., 199641 Unknown Satisfactory Unknown Additional surgery was
performed to level out
the occlusal plane
L, left; R, right; F, female; M, male; preop., preoperative; postop., postoperative; TMJ, temporomandibular joint; RDC/TMD, Research Diagnostic
Criteria for Temporomandibular Disorders; MIO, maximum inter-incisal opening; SPECT, single photon emission computed tomography; CT,
computed tomography; VAS, visual analogue scale; GCP, graded chronic pain scale; HC, high condylectomy; OS, orthognathic surgery; T6, at
least 12 months post surgery; BSSO, bilateral sagittal split osteotomy.
a
For determining activity.

pantomogram examination has also been
questioned by Türp et al.54
Most articles did not contain a system-
atic registration of the TMJ symptoms
prior to and following surgery; however,
almost all reviewed articles mentioned an
improvement in TMJ symptoms, such as
reduced swelling, trismus, and pain, when
outcomes were compared to the presurgi-
cal clinical findings. Furthermore, Villa-
nueva-Alcojol et al.47 found an association
between histological type and the TMJ
symptoms observed. In their study, a sam-
ple of 18 patients was categorized accord-
ing to the histological classification of
Slootweg and Müller, i.e. condylar hyper-
plasia types I, II, III, and IV (see Fig. 4).
No possible association was found be-
tween patient age and histological type
as has been suggested by Slootweg and
Müller. However in those patients with
type I condylar hyperplasia, no patient
had TMJ problems. All those with type
II condylar hyperplasia had TMJ symp-
toms like clicking/pain, and those with
type III condylar hyperplasia showed a
mixed representation of TMJ appearance.
Only the article by Appel et al.39 sug-
gested that the patients had worsening
of various TMJ conditions following high
condylectomy when compared to preop-
erative levels.
In most articles, the risk of nerve dam-
age during the high condylectomy proce-
dure was not recorded; in one article, no
nerve damage occurred during the proce-
dure,42 while in another article, it was
mentioned that one patient sustained dam-
age to the auriculotemporal nerve.39 One
article addressed psychological issues in
detail: Saridin et al.46 reported that the
presence of psychological problems like
depression amongst patients treated with a
high condylectomy was almost the same
as in the control group and that psychologi-
cal problems do not need to be taken into
consideration when planning treatment.
Ten of the 11 articles suggested that
the high condylectomy procedure is an
efficient way to deal with MCH.4,5,40–47
Nine of the articles described the amount
of bone that was removed during surgery,
which ranged from 1.5 to 7 mm.39,5,40,42–
44,46,47
In one article, the high condylect-
omy was described as being unsuccessful,
and hence was suggested as not being a
relevant treatment option for MCH.39
Risk of bias
The assessment of the risk of bias is pre-
sented in Table 2. All clinical trials in-
cluded in the study appeared to have
recruited patients more or less consecu-
tively; however, most trials did not state
this directly. No attempt was made to
68 Ghawsi et al.

Histological classificaon of condylar hyperplasia by Slootweg and Müller

Type I Broad proliferaon zone. Underlying thick layer of hyaline growth carlage. Bone
containing numerous carlage islands.

Type II Patchy distribuon (cell-rich areas alternang with non-proliferave cell-poor

zones). Carlage islands in cancellous bone are less frequent than in type 1.

Type III Great distoron. Irregularly shaped masses of hyaline carlage extending into
cancellous bone of condylar neck or encroaching upward onto superficial arcular layer.

Type IV Connuous subchondral bone plate covered by cell-poor fibrocarlaginous layer.

No proliferaon layer of hyaline growth cartilage. Burned-out appearance of the condyle.

Fig. 4. Histological classification of condylar hyperplasia by Slootweg and Müller.

conceal allocation by the clinical trials.
Overall, the risk of selection bias was
considered low.
With regard to the risk of performance
bias, most studies were not blinded and the
examiners were aware of the presence of
CH in patients classified by the different
classification systems based on clinical ap-
pearance. Only three studies included a
control group; however, it was not men-
tioned whether these clinical trials were
blinded or not.4,5,46 In one study, the clini-
cal examiner was an uninvolved trained
examiner.46 Overall, the risk of this
bias was therefore considered moderate
to high.
The risk of detection bias was not evalu-
ated because most trials did not have a
control group and/or did not address wheth-
er the examiner/surgeon was blinded.
A total of 14 patient drops-outs
from two different clinical trials were
identified.39,46 Furthermore, 18 patients
were excluded in another clinical trial
due to inconsistent data.47 Relating
this to the total number of 289 patients,
the risk of attrition bias was considered
low.
The risk of reporting bias was unclear in
all the trials included.
Discussion
This review aimed to highlight the rele-
vance of high condylectomy in patients
diagnosed with MCH. However, the liter-
ature reviewed was inconsistent with re-
gard to how to diagnose and treat MCH
(UCH).
Unfortunately, only limited information
on the aetiology of MCH is available.
However, several classification systems
have been suggested to categorize the
clinical, radiological, and histological
findings in MCH. Most authors seem to
agree on the distinction between two types
of MCH, i.e., the idiopathic type of MCH
and MCH of known aetiology.
Also, most studies suggest that there is no
difference between the sexes or between
ethnic groups with regard to the prevalence
of MCH.51,52 However, it was found that
there were more women than men in the
studies reviewed here. Whether this is a
result of more women seeking treatment
than men remains unknown.
In 99% of the population, facial growth
is completed at the age 15 years in females
and at the age of 18 years in males. It has
been reported that the yearly growth rate
of the mandible from condylion to B-point
is 1.6 mm in females and 2.2 mm in
males.55 Thus, a normal condyle is 15–
20 mm in mediolateral dimension and 8–
10 mm in anterior–posterior dimension.56
An accelerated deviation from this might
indicate MCH.57 However, all authors in
this review emphasized the need to ex-
clude other relevant diagnoses before a
diagnosis of MCH is made because of
the idiopathic aetiology of the condi-
tion.4,5,39–47 The differential diagnosis

Differenal diagnosis for mandibular condylar hyperplasia type 1 according to Wolford et al.

1. Maxillary hypoplasia

2. Mandibular prognathism without mandibular condylar hyperplasia

3. Dislocaon of condyles anterior to the arcular eminence

4. Dental interferences or habitual posturing causing anterior posioning of the

mandible

5. Acromegaly

6. Macroglossia

7. Congenital or accurate facial asymmetry unrelated to the temporomandibular joint

8. Other TMJ pathology such as osteochondroma, osteoma, or contralateral condylar

resorpon

Fig. 5. The differential diagnosis for condylar hyperplasia type 1 according to Wolford et al.
 High condylectomy for the treatment of MCH 69

Table 2. Assessment of the risk of bias.

Reporting:
Selection: Detection: Attrition: difference
consecutive or Performance: blinded blinded to HC or dropouts and between reported
Study randomized to CH actual outcome exclusions and actual
Chiarini et al., 201442 Not specified No, all patients No blinding No dropouts, no Not mentioned,
(2005–2012) classified according to measures exclusions no evidence of
Wolford’s mentioned such bias
classification system
Jones and Tier, 201244 Consecutive No, all patients selected No blinding No dropouts, no Not mentioned,
according to Wolford’s measures exclusions no evidence of
classification system mentioned such bias
Villanueva-Alcojol Not specified No, knowledge of No blinding No dropouts, Not mentioned,
et al., 201147 (1998–2009) excessive unilateral measures only 18/36 no evidence of
growth resulting in mentioned histopathological such bias
asymmetry according cases were
to Obwegeser and classified
Makek according to
Slootweg and
Müller
Saridin et al., 201046 Not specified Yes, clinical Unclear 13 dropouts, no Not mentioned,
(1994–2007) examination performed exclusions no evidence of
by one uninvolved such bias
researcher
Brusati et al., 201040 Not specified Not specified Not specified No dropouts Not mentioned,
(1998–2007) (however one no evidence of
patient refused to such bias
undergo
functional
rehabilitation),
no exclusions
Wolford et al., 20095 Not specified Not specified, included Unclear, No dropouts, no Not mentioned,
(prior to 2000) a control group however a exclusions no evidence of
control group such bias
was present
Deleurant et al., 200843 Not specified Not specified Not specified, No dropouts, no Not mentioned,
(1997–2007) only one surgeon exclusions no evidence of
performed such bias
surgery
Lippold et al., 200745 Not specified Not specified Not specified No dropouts, no Not mentioned,
(2000–2004) exclusions no evidence of
such bias
Wolford et al., 20024 Not specified Not specified, included Not specified, No dropouts, no Not mentioned,
a control group however one exclusions no evidence of
control group such bias
included and one
surgeon
performed
surgery
Appel et al., 199739 Not specified Not specified Not specified 1 dropout, no Not mentioned,
(1983–1992 in exclusions no evidence of
Hannover and such bias
1993–1995 in
Bonn)
Chen et al., 199641 Not specified Not specified, however Not specified No dropouts, no Not mentioned,
(1982–1993) patients included exclusions no evidence of
classified according to such bias
Obwegeser and Makek
Risk of bias Low risk Moderate–high risk Unclear Low risk Unclear
CH, condylar hyperplasia; HC, high condylectomy.

for condylar hyperplasia type 1 according
to Wolford et al. is illustrated in Fig. 5.
The studies in this review focused on the
activity of mandibular condylar growth,
UCH being described as a dynamic process.
Furthermore, Wolford et al. have suggested
that CH1 presents at an early age.
The diagnostic tools used to identify
MCH and/or UCH are mainly clinical
records, clinical photographs, and conven-
tional cephalograms. Some authors have
described histological findings in various
classification systems. However, it has
been postulated in recent studies that
the histological findings are unspecific
to the pathological appearance of
MCH.31 Also, the use of SPECT has been
discussed, with some authors suggesting
that the lack of classical findings means
that SPECT provides only limited addi-
tional information on the pathological
70 Ghawsi et al.
TMJ changes. Wolford et al. have also
stated that SPECT scintigraphy is unnec-
essary in the diagnosis of UCH, because
the findings are inconclusive in younger
patients and in patients with slowly evolv-
ing MCH. Saridin et al. have suggested
that the newer positron emission tomog-
raphy techniques may represent a useful
diagnostic tool.58
The majority of the articles suggested
early intervention because UCH may be
caused by a hyperactive growth centre.
Early intervention ensures a minimum
amount of intervention, and in addition,
if UCH is treated at the appropriate time,
excellent aesthetic and functional results
can be obtained in combination with or-
thodontics. Wolford et al. have suggested
intervention for MCH at age 14 years in
females and 16 years in males, although
when unilateral, the procedure can be
delayed until age 15 years in females
and 17–18 years in males, sometimes in
combination with orthognathic surgery.
Interestingly, in the two studies by Wol-
ford et al. it was shown that there was a
100% setback relapse in the condyles and
the need for a second corrective surgical
intervention at a later date in the control
group, in which the patients only under-
went orthognathic surgery to correct their
facial asymmetry. However, in the group
of patients with facial asymmetry due to
MCH who underwent both orthognathic
surgery and a high condylectomy, no
relapses were seen.4,5 This illustrates
the importance of diagnosing MCH and
ensuring correct treatment options to ad-
dress this specific problem in order to
guarantee that the outcome of the surgical
intervention provides adequate function
and aesthetics.
In most studies, the minimum amount of
bone excised was 3 mm; the maximum
was 7 mm, plus a little contouring of the
remaining condylar head. This is in accor-
dance with most recommendations made
on the basis of prior experience with the
high condylectomy, which range from 5 to
7 mm.31,39 Only one article reported un-
successful outcomes, but only 1.5–3 mm
was excised in that study.39 In most stud-
ies, other types of surgery, such as the
bilateral sagittal split osteotomy, Le Fort I,
and costochondral graft, had to be used in
addition to the high condylectomy to
achieve optimal aesthetic and functional
results.
In terms of TMJ and general discomfort
after the procedure, there were no note-
worthy differences between the treated
and control groups in those articles that
included a control group. One article,
however, did mention that the symptoms
worsened after the procedure, making it
necessary to undergo a secondary correc-
tive phase.39 More accurate postoperative
data are needed before this matter can be
discussed further.
The overall risk of bias for the assess-
ment outcome was regarded to be moder-
ate. There are difficulties in designing
blinded clinical trials for these types of
study, because a specific problem – MCH
– is being addressed with a specific treat-
ment option – the high condylectomy.
However, this obstacle can be overcome
with the inclusion of control groups, as
Wolford et al. did in their clinical trials.4,5
A better description of patient selection,
blinded studies, and a full description of
the protocol are necessary to enable better
future systematic reviews on this subject.
This review confirmed that the high
condylectomy is a successful procedure
in patients with MCH caused by an accel-
eration of the normal growth mechanism.
Unfortunately, no definite approach to the
clinical and paraclinical diagnosis of con-
dylar hyperplasia was available in the
studies reviewed. However, a combination
of clinical examinations over a period of
6 months to 1 year, dental casts, clinical
photographs, panoramic radiographs,
SPECT scans, and cephalograms aids in
making a correct diagnosis. In addition,
there is no absolute agreement regarding
the optimum timing of intervention or the
amount of bone that needs to be excised to
prevent further growth. Most articles sug-
gest early intervention, with the excision
of a least 3–6 mm of bone for a successful
result. Also, the procedure can be under-
taken at an early age, thereby minimizing
the need for secondary aesthetic interven-
tions and securing a better functional re-
sult in younger patients. Further studies
with more precise data are needed to
elaborate on and make recommendations
concerning the exact timing of the inter-
vention and the amount of excision nec-
essary.
Funding
None.
Competing interests
None.
Ethical approval
Not needed.
Patient consent
Not needed.
References
1. Adams R. A treatise on rheumatic gout or
chronic rheumatic arthritis of all joints. 2nd
ed. London: Churchill; 1873: 271.
2. Bruce RA, Hayward JR. Condylar hyperpla-
sia and mandibular asymmetry: a review. J
Oral Surg 1968;26:281–90.
3. Norman JE, Painter DM. Hyperplasia of the
mandibular condyle. A historical review of
important early cases with a presentation and
analysis of twelve patients. J Maxillofac
Surg 1980;8:161–75.
4. Wolford LM, Mehra P, Reiche-Fischel O,
Morales-Ryan CA, Garcı́a-Morales P. Effi-
cacy of high condylectomy for management
of condylar hyperplasia. Am J Orthod Den-
tofacial Orthop 2002;121:136–50. discus-
sion 150–1.
5. Wolford LM, Morales-Ryan CA, Garcı́a-
Morales P, Perez D. Surgical management
of mandibular condylar hyperplasia type 1.
Proc (Bayl Univ Med Cent) 2009;22:321–9.
6. Kaban LB. Mandibular asymmetry and the
fourth dimension. J Craniofac Surg
2009;20:622–31. http://dx.doi.org/10.1097/
SCS.0b013e318195249c.
7. Rushton MA. Growth at the mandibular
condyle in relation to some deformities. Br
Dent J 1944;76:57–68.
8. Rushton MA. Unilateral hyperplasia of
the jaws in the young. Int Dent J 1951;2:
41–76.
9. Jacobsen PU, Lund K. Unilateral overgrowth
and remodeling processes after fracture of
the mandibular condyle: a longitudinal ra-
diographic study. Scand J Dent Res
1972;80:68–74.
10. Gordon S, Antoni A, Booker RE. Acquired
unilateral condylar hypertrophy. J Can Dent
Assoc 1957;23:76–80.
11. Burch RJ, Shuttee TS. Unilateral hyperplasia
of left mandibular condyle and hypoplasia of
body of right side of mandible: report of
case. J Oral Surg Anesth Hosp Dent Serv
1960;18:255–8.
12. Hyckel P, Erler U, Müller P. Unilateral hy-
perplasia of the TMJ condyle. Dtsch Z
MundKiefer Gesichtschir 1991;15:42–50.
13. Lineaweaver W, Vargervik K, Tomer BS,
Ousterhout DK. Posttraumatic condylar hy-
perplasia. Ann Plast Surg 1989;22:163–72.
14. Gruca A, Meisels E. Asymmetry of the
mandible from unilateral hypertrophy. Ann
Surg 1926;83:755–67.
15. Thoma KH. Hyperostosis of the mandibular
condyle with report of two cases. Oral Surg
1945;31:597–607.
16. Gottlieb O. Hyperplasia of the mandibular
condyle. J Oral Surg 1951;9:118–35.
17. Rowe NL. Aetiology clinical features and
treatment of mandibular deformity. Br Dent
J 1960;108:41–64.
18. Walker RV. Condylar abnormalities. Trans
Int Conf Oral Surg 1967:81–96.
19. Egyedi P. Aetiology of condylar hyperplasia.
Aust Dent J 1969;14:12–7.

20. Oberg T, Fajers CM, Lysell G, Friberg U.
Unilateral hyperplasia of the mandibular con-
dylar process. A histological, microradiograph-
ic, and autoradiographic examination of one
case. Acta Odontol Scand 1962;20:485–504.
21. Yang J, Lignelli JL, Ruprecht A. Mirror
image condylar hyperplasia in two siblings.
Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 2004;97:281–5. http://
dx.doi.org/10.1016/S1079210403005560.
22. Slootweg PJ, Müller H. Condylar hyperpla-
sia. A clinico-pathological analysis of 22
cases. J Maxillofac Surg 1986;14:209–14.
23. Saridin CP, Raijmakers P, Becking AG. Quan-
titative analysis of planar bone scintigraphy in
patients with unilateral condylar hyperplasia.
Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 2007;104:259–63. http://dx.doi.org/
10.1016/j.tripleo.2006.08.018.
24. Wolford LM, LeBanc J. Condylectomy to
arrest disproportionate mandibular growth.
Presentation at the American Cleft Palate
Association Meeting. 1985.
25. Obwegeser HL, Makek MS. Hemimandibu-
lar hyperplasia—hemimandibular elonga-
tion. J Maxillofac Surg 1986;14:183–208.
26. Wolford LM, Movahed R, Perez D. A clas-
sification system for conditions causing con-
dylar hyperplasia. J Oral Maxillofac Surg
2014;72:567–95. http://dx.doi.org/10.1016/
j.joms.2013.09.002.
27. De Bont LG, Boering G, Liem RS, Eulderink
F, Westesson PL. Osteoarthritis and internal
derangement of the temporomandibular
joint: a light microscopic study. J Oral Max-
illofac Surg 1986;44:634–43.
28. Hansson T, Oberg T, Carlsson GE, Kopp S.
Thickness of the soft tissue layers and the
articular disk in the temporomandibular
joint. Acta Odontol Scand 1977;35:77–83.
29. Richards LC, Lau E, Wilson DF. Histopa-
thology of the mandibular condyle. J Oral
Pathol 1985;14:624–30.
30. Eslami B, Behnia H, Javadi H, Khiabani KS,
Saffar AS. Histopathologic comparison of
normal and hyperplastic condyles. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod
2003;96:711–7. http://dx.doi.org/10.1016/
S1079210403003792.
31. Hodder SC, Rees JI, Oliver TB, Facey PE,
Sugar AW. SPECT bone scintigraphy in the
diagnosis and management of mandibular
condylar hyperplasia. Br J Oral Maxillofac
Surg 2000;38:87–93. http://dx.doi.org/
10.1054/bjom.1999.0209.
32. Bohuslavizki KH, Brenner W, Kerscher A,
Fleiner B, Tinnemeyer S, Sippel C, et al.
The value of bone scanning in pre-operative
decision-making in patients with progressive
facial asymmetry. Nucl Med Commun
1996;17:562–7.
33. Cisneros GJ, Kaban LB. Computerized skel-
etal scintigraphy for assessment of mandib-
ular asymmetry. J Oral Maxillofac Surg
1984;42:513–20.
34. Pogrel MA. Quantitative assessment of iso-
tope activity in the temporomandibular joint
High condylectomy for the treatment of MCH
regions as a means of assessing unilateral
condylar hypertrophy. Oral Surg Oral Med
Oral Pathol 1985;60:15–7.
35. Laverick S, Bounds G, Wong WL. [18F]-
fluoride positron emission tomography for
imaging condylar hyperplasia. Br J Oral
Maxillofac Surg 2009;47:196–9. http://
dx.doi.org/10.1016/j.bjoms.2008.08.001.
36. Hampf G, Tasanen A, Nordling S. Surgery in
mandibular condylar hyperplasia. J Maxillo-
fac Surg 1985;13:74–8.
37. Moher D, Liberati A, Tetzlaff J, Altman DG.
Preferred reporting items for systematic
reviews and meta-analyses: the PRISMA
statement. Int J Surg 2010;8:336–41.
http://dx.doi.org/10.1016/j.ijsu.2010.02.007.
38. Higgins JP, Altman DG, Sterne JA. Asses-
sing risk of bias in included, studies. In:
Higgins J, Green S, editors. Cochrane hand-
book for systematic reviews of interventions,
version, 5., 1., 0 (updated March, 2011).
The Cochrane Collaboration; 2011.
39. Appel T, Niederhagen B, Braumann B,
Reich RH. High condylectomy for control
of pathological growth in condylar hyperpla-
sia. Mund Kiefer Gesichtschir
1997;1(Suppl):S138–40.
40. Brusati R, Pedrazzoli M, Colletti G. Func-
tional results after condylectomy in active
laterognathia. J Craniomaxillofac Surg
2010;38:179–84. http://dx.doi.org/10.1016/
j.jcms.2009.04.010.
41. Chen YR, Bendor-Samuel RL, Huang CS.
Hemimandibular hyperplasia. Plast
Reconstr Surg 1996;97:730–7.
42. Chiarini L, Albanese M, Anesi A, Gal-
zignato PF, Mortellaro C, Nocini P, et al.
Surgical treatment of unilateral condylar
hyperplasia with Piezosurgery. J Craniofac
Surg 2014;25:808–10. http://dx.doi.org/
10.1097/SCS.0000000000000699.
43. Deleurant Y, Zimmermann A, Peltomäki T.
Hemimandibular elongation: treatment and
long-term follow-up. Orthod Craniofac Res
2008;11:172–9. http://dx.doi.org/10.1111/
j.1601-6343.2008.00427.x.
44. Jones RH, Tier GA. Correction of facial
asymmetry as a result of unilateral condylar
hyperplasia. J Oral Maxillofac Surg
2012;70:1413–25. http://dx.doi.org/
10.1016/j.joms.2011.03.047.
45. Lippold C, Kruse-Losler B, Danesh G, Joos
U, Meyer U. Treatment of hemimandibular
hyperplasia: the biological basis of condy-
lectomy. Br J Oral Maxillofac Surg
2007;45:353–60. http://dx.doi.org/10.1016/
j.bjoms.2006.10.011.
46. Saridin CP, Gilijamse M, Kuik DJ, te Veld-
huis EC, Tuinzing DB, Lobbezoo F, et al.
Evaluation of temporomandibular function
after high partial condylectomy because of
unilateral condylar hyperactivity. J Oral
Maxillofac Surg 2010;68:1094–9. http://
dx.doi.org/10.1016/j.joms.2009.09.105.
47. Villanueva-Alcojol L, Monje F, González-
Garcı́a R. Hyperplasia of the mandibular con-
dyle: clinical, histopathologic, and treatment
71
considerations in a series of 36 patients. J Oral
Maxillofac Surg 2011;69:447–55. http://
dx.doi.org/10.1016/j.joms.2010.04.025.
48. Iannetti G, Cascone P, Belli E, Cordaro L.
Condylar hyperplasia: cephalometric study,
treatment planning, and surgical correction
(our experience). Oral Surg Oral Med Oral
Pathol 1989;68:673–81.
49. Nitzan DW, Katsnelson A, Bermanis I, Brin I,
Casap N. The clinical characteristics of con-
dylar hyperplasia: experience with 61 patients.
J Oral Maxillofac Surg 2008;66:312–8. http://
dx.doi.org/10.1016/j.joms.2007.08.046.
50. Motamedi MH. Treatment of condylar hy-
perplasia of the mandible using unilateral
ramus osteotomies. J Oral Maxillofac Surg
1996;54:1161–9. discussion 1169- 1170.
51. Henderson MJ, Wastie ML, Bromige M,
Selwyn P, Smith A. Technetium-99m bone
scintigraphy and mandibular condylar hy-
perplasia. Clin Radiol 1990;41:411–4.
52. Matteson SR, Proffit WR, Terry BC, Staab
EV, Burkes EJ. Bone scanning with 99m
technetium phosphate to assess condylar
hyperplasia. Report of two cases. Oral Surg
Oral Med Oral Pathol 1985;60:356–67.
53. Gray RJ, Sloan P, Quayle AA, Carter DH.
Histopathological and scintigraphic features
of condylar hyperplasia. Int J Oral Maxillo-
fac Surg 1990;19:65–71.
54. Türp JC, Vach W, Harbich K, Alt KW, Strub
JR. Determining mandibular condyle and
ramus height with the help of an orthopan-
tomogram—a valid method? J Oral Rehabil
1996;23:395–400.
55. Riolo ML, Moyers RE, McNamara JA,
Hunter WS. An atlas of craniofacial growth:
cephalometric standards from the University
School Growth Study. Ann Arbor, MI: The
University of Michigan, University of Michi-
gan; 1974: 105–6.
56. Lindblom G. On the anatomy and function of
the temporomandibular joint. Acta Odontol
Scand 1960;17:23–7.
57. Kerstens HC, Tuinzing DB, Golding RP, van
der Kwast WA. Condylar atrophy and osteoar-
throsis after bimaxillary surgery. Oral Surg
Oral Med Oral Pathol 1990;69:274–80.
58. Saridin CP, Raijmakers PG, Kloet RW, Tuinz-
ing DB, Becking AG, Lammertsma A. No
signs of metabolic hyperactivity in patients
with unilateral condylar hyperactivity: an in
vivo positron emission tomography study. J
Oral Maxillofac Surg 2009;67:576–81. http://
dx.doi.org/10.1016/j.joms.2008.09.021.
Address:
Sodaba Ghawsi
Department of Oral and Maxillofacial
Surgery
Odense University Hospital
Sdr. Boulevard 29
5000 Odense C
Denmark
Tel: +45 28739306
E-mail: ghawsi@hotmail.com