REVIEW ARTICLE

Treatment of Mandibular Prognathism

Hong-Po Chang,* Yu-Chuan Tseng, Hsin-Fu Chang1

Mandibular prognathism (MP) or skeletal Class III malocclusion with a prognathic mandible is one of the
most severe maxillofacial deformities. Facial growth modification can be an effective method of resolvingg
skeletal Class III jaw discrepancies in growing children with dentofacial orthopedic appliances includingg
the chincup, face mask, maxillary protraction combined with chincup traction and the Fränkel functional
regulator III appliance. Orthognathic surgery in conjunction with orthodontic treatment is required for the
correction of adult MP. The two most commonly applied surgical procedures to correct MP are sagittal splitt
ramus osteotomy (SSRO) and intraoral vertical ramus osteotomy. Both procedures are suitable for patients
in whom a desirable occlusal relationship can be obtained with a setback of the mandible, and each has its
own advantages and disadvantages. In bilateral SSRO, the intentional ostectomy of the posterior part of the
distal segment can offer long-term positioned stability. This may be attributable to reduction of tension in
the pterygomasseteric sling that applies force in the posterior mandible. While various environmental factors
have been found to contribute to the development of MP, heredity plays a substantial role. The relative con-
tributions of genetic and environmental components in the etiology of MP are unclear. The recent identifi-
cation of the genetic susceptibilities to MP constitutes the first step toward understanding the molecularr
pathogenesis of MP. Further studies in molecular biology are needed to identify the gene–environmentt
interactions associated with the phenotypic diversity of MP and the heterogenic developmental mechanisms
thought to be responsible for them. [J Formos Med Assoc 2006;105(10):781–790]

Key Words: dentofacial orthopedics, environmental factors, genetics, mandibular prognathism,

morphogenetic basis, orthognathic surgery

In the early 1900s, Angle,1 the father of modern from 15% to 23%, has been observed in Asian
orthodontics, described three basic types of mal- Mongoloid populations of Taiwanese, Japanese,
occlusion for dental occlusion: Class I, II and III Korean and Chinese.3–6 In contrast, most studies
malocclusions. Class III malocclusion is defined reported an incidence of this class of malocclu-
by the mandibular first permanent molar being sion in American, European and African Caucasian
“mesial”, i.e. forward to normal in its relation- populations below 5%.7–9 Class III malocclu-
ship with the maxillary first molar. Lischer2 later sion is thus a common clinical problem in
termed Angle’s Class III malocclusion as mesio- orthodontic patients of Asian or Mongoloid
occlusion. This method of categorization, however, descent.10–12
does not provide information about the devel- Studies indicate that 63–73% of Class III mal-
opmental mechanisms by which the observed occlusions are of skeletal type.4,13 Such skeletal
occlusal relationship has been reached. A rela- cases result from growth disharmony between the
tively high prevalence of Class III malocclusion, mandible and maxilla, thus producing a concave

©2006 Elsevier & Formosan Medical Association

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Department of Orthodontics, Kaohsiung Medical University Hospital and Faculty of Dentistry and Graduate Institute of Dental Sciences,
College of Dental Medicine, Kaohsiung, and 1Department of Orthodontics, National Taiwan University Hospital and School of Dentistry,
National Taiwan University College of Medicine, Taipei, Taiwan.

Received: January 5, 2006 *Correspondence to: Dr Hong-Po Chang, Department of Orthodontics, Kaohsiung Medical University,
Revised: February 14, 2006 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan.
Accepted: April 4, 2006 E-mail: hopoch@kmu.edu.tw

J Formos Med Assoc | 2006 • Vol 105 • No 10 781

H.P. Chang, et al
facial profile. Patients with skeletal Class III mal-
occlusion can exhibit mandibular protrusion,
maxillary retrusion or a combination of the two.4,8
Mandibular prognathism (MP) or skeletal Class III
malocclusion with a prognathic mandible has long
been viewed as one of the most severe maxillo-
facial deformities.9
The etiologic factors of this skeletal type of
Class III malocclusion have not been fully unrav-
eled, remain incompletely understood, and the re-
gions of the craniofacial complex that are affected
by various treatment modalities have not been
delineated explicitly. The aims of this review are
to rationalize morphologic and etiologic compo-
nents and to identify areas where further research
is needed to fully delineate the basis of MP and its
clinical management.
Maxillofacial Complex in MP
Cephalometric and geometric morphometric
studies14–19 have shown that the deformations in
subjects with Class III malocclusion may represent
a developmental shortening of the palatomaxillary
complex and elongation of the mandible antero-
posteriorly, which leads to the appearance of a
retrognathic midface and prognathic mandibular
profile.
MP may be due to a hypoplastic and/or retro-
positioned maxilla, a greater total length and an-
terior positioning of the mandible.17 Our previous
study in adults showed that the position of the
maxilla relative to the anterior cranial base
showed no significant difference between MP
and normal occlusion groups.18 Nevertheless, there
were significantly shorter palatal and maxillary
lengths in the prognathic group. The total length
and anterior positioning of the mandible are
particularly suitable criteria for the differential di-
agnostic evaluation of MP, as revealed by discrim-
inant analysis.17 The midfacial deformations may
represent a developmental diminution of the pala-
tomaxillary complex anteroposteriorly that allies
with the vertical shortening of midfacial height an-
teriorly.18 The changes in mandibular morphology
782
noted for this skeletal Class III deformity may re-
present a developmental elongation of the man-
dible anteroposteriorly, leading to the appearance
of a prognathic facial profile.18–20
Morphogenetic Basis for MP
The results of studies of the cranial base in subjects
with Class III malocclusion and MP compared
with normal occlusion controls showed that the
greatest between-group differences occurred in the
posterior cranial base region.18,21 It was concluded
that shortening and angular bending of the cranial
base, and a diminished angle between the cranial
base and ascending ramus, may be associated with
the formation of MP, and with the appearance of a
Class III facial morphology of retrognathic midface
and/or prognathic mandible.18,21 Besides the more
acute articular or saddle angle in the cranial base,
individuals with MP had a more obtuse fronto-
nasal angle, presumably associated with a retrusive
midfacial profile.21
The shape of the cranial base appears to be es-
tablished during fetal development,22–24 and re-
mains relatively stable during postnatal growth.25,26
Kerr27 found that saddle angle was one of the few w
craniofacial parameters that varied little duringg
the growth period from 5 to 15 years of age.
An extensive longitudinal study by Bhatia and
Leighton28 confirmed such stability in both sexes,
although there was wide interindividual variabil-
ity. A prominent feature of this early growth is
progressive flattening of the cranial base duringg
late prenatal development.22,23,29,30 Therefore, a
Class III cranial base morphology may be estab-
lished very early in development, possibly at the
prenatal stage.31 Moreover, a Class III morphologyy
may arise, not because of increased cranial base
flexion, but rather because of deficient ortho-
cephalization, or failure of the cranial base to flat-
ten anteroposteriorly. However, cranial base flexure
is not the only factor involved in determining mal-
occlusion. Scott32,33 suggested that several factors
determine or influence the jaw position and, con-
sequently, occlusion in individual cases. The three
J Formos Med Assoc | 2006 • Vol 105 • No 10

principal factors involved are the cranial base angle,
the extent to which the mandible and maxilla are
moved forward in relation to the cranium, and the
amount of surface bone deposition along the
facial profile from nasion to menton.32,33
The anterior cranial base provides the template
that establishes the horizontal length of the mid-
facial complex, which is also relatively short in
Class III malocclusion.34 Therefore, the cranial
base has a role in the final positioning of the mid-
face and mandible that could account for the clin-
ical presentation of mandibular protrusion and/or
maxillary retrusion in individuals with MP. How-
ever, conflicting data in the literature35–37 suggest
that anterior cranial base length might not play
an important role in the pathogenesis of Class III
malocclusion. The nasion may be quite variable
in its position during growth and, thus, may con-
tribute to the contradictory findings.37,38 Another
possible explanation for such findings is that the
foramen cecum of frontal bone is the anterior ana-
tomic limit of the anterior cranial base,39 and the
nasion may not be appropriate for characterizing
anterior cranial base configuration.
Decreased angulation between the anterior
and posterior cranial bases, particularly associated
with the articulare (Ar), was also noted in studies
of adults with MP and children with Class III
malocclusion. Thus, anterior displacement of the
temporomandibular joint appears to be demon-
strable in subjects with Class III malocclusion and
MP. The resulting prognathic face, characterized
by shortening and angular bending of the cranial
base, and a diminished angle between the cranial
base and mandibular ramus,40 provides an indi-
cation of apparent cranial base kyphosis, associ-
ated with the appearance of a Class III facial
morphology.
Ethnic Variations in Craniofacial Form:
Structural Basis of Basicranium for MP
Class III malocclusion shows a relatively low
prevalence in Caucasian populations, whereas its
prevalence has been observed to be much higher
J Formos Med Assoc | 2006 • Vol 105 • No 10
Treatment off mandibular prognathism
in Asians. Our analysis of local differences in
cranial base configuration on cephalographs be-
tween European–American and four Asian groups
(Taiwanese, Japanese, Korean, Chinese) in youngg
adults with normal Class I molar occlusion, usingg
thin-plate spline and strain tensor graphical
analyses,41 showed that the greatest differences
occurred in the anterior portion of the cranial base
and upper midface region, which generally con-
sisted of horizontal compression. The posterior-
most cranial base region also showed horizontal
compression between the Bolton point (Bo) and
Ar with forward compression of the Ar. This
represented frontal and facial flatness (the char-
acteristic feature of Asian faces)42–44 and anteriorr
displacement of the temporomandibular joint.
These findings indicated that the composite resultt
is a relative retrusion of the nasomaxillary com-
plex and a more forward relative placement of the
mandible. This results in a greater tendency toward
a prognathic mandible and/or retrognathic mid-
face and a Class III type of malocclusion in Asian
populations. Therefore, it appears that Class III
malocclusions are prevalent to a greater degree in
Asian populations and even Class I and II cases
may exhibit an underlying Class III character.45,46
Etiologic Factors of MP
Heredity of MP
MP is one of the best-known facial genetic traits
or phenotypes. It is also well recognized that eth-
nicity is a risk factor for MP; the highest incidence
has been observed in Asian populations and the
lowest in Caucasian populations as previously dis-
cussed. The existence of familial aggregation of MP
suggests that genetic components play an impor-
tant role in its etiology. Numerous studies have
shown a significantly higher incidence of this phe-
notype in the relatives of affected probands.47–50
In the offspring of affected parents, extensive stud-
ies of Japanese families showed a frequency of 31%
if the father was affected, 18% if the mother was
affected and 40% if both parents were affected.47,51
In siblings of affected probands, Litton et al52
783
H.P. Chang, et al
found a frequency of 13% irrespective of sex.
Concordance for MP among twin pairs collected
from published reports was 81.0–83.3% for
monozygotic and 10.0–13.3% for dizygotic twin
pairs.53,54 However, the inheritance pattern of
MP is controversial; findings have been reported
suggesting autosomal-recessive inheritance,47,55
autosomal-dominant inheritance,49,56 dominant
inheritance with incomplete penetrance48,57,58 or
a polygenic model of transmission.52
The Habsburgs, one of Europe’s foremost royal
families, are famous not only for the duration of
their reign and brilliance of their leadership, but
also because they represent one of the few exam-
ples of the inheritance patterns of facial char-
acteristics. The term “Habsburg jaw” has been
coined to describe the prognathic mandible seen
in 23 successive generations of this family.57,59,60
Males were more severely affected than females.
The facial characteristics of the royal Habsburgs
included MP, thickened lower lip, prominent, often
misshapen nose, flat malar areas (maxillary hy-
poplasia) and mildly everted lower eyelids.57,59,60
The Habsburgs suffered from various other ail-
ments including asthma, gout, dropsy, epilepsy
and melancholia. The early Habsburgs were unfor-
tunate enough to not have been acquainted with
the laws of heredity and the consequences of con-
sanguineous marriage or inbreeding.
Although there appears to be a strong familial
tendency in the development of MP, the rate of
developing MP in patients with a positive family
background (49.3%) is not higher than those with
a negative one (50.7%).61 Therefore, the preva-
lence of MP may depend on candidate genes being
expressed, with gene–environment interactions
determining the severity of MP. The relative con-
tributions of genetic and environmental compo-
nents in the etiology of MP are unclear. Little is
known about the interaction between genetic and
environmental factors in the causation of MP.
Recent progress in molecular genetics has en-
abled the genetic determinant to be approached
directly. Yamaguchi et al62 performed a genome-
wide linkage analysis identifying three chromo-
somal loci (including 1p36, 6q25 and 19p13.2)
784
susceptible to MP with 90 affected sibling pairs
from 50 Japanese and 40 Korean populations.
The replication of these results with an inde-
pendent dataset should facilitate the positional
cloning of the gene or genes that influence the
development of MP. Therefore, large-scale studies
of well-defined families, including those of otherr
ethnicities, are warranted to confirm the evidence
of linkage to MP.
Environmental factors associated with MP
Various environmental factors have been found
to contribute to the development of MP, inclu-
ding congenital anatomic defects (cleft lip–cleftt
palate),63,64 endocrine disturbance (acromegaly,
gigantism, pituitary adenomas),20,55,63,65,66 naso-
airway obstruction (enlarged tonsils),20,67 habitual
posture (habit of protruding the mandible)23,70
and trauma (instrumental deliveries).68,69
Determination of tongue position is impor-
tant in the diagnosis of certain clinical conditions,
such as MP, dentoalveolar crossbite or bialveolarr
protrusion of teeth. These clinical conditions can
be associated with forward tongue position and/orr
enlarged tonsils.20,67 A lower pharyngeal width off
more than 15 mm suggests anterior positioningg
of the tongue, either as a result of habitual pos-
ture or due to an enlargement of the tonsils.67 The
lower pharyngeal width is measured from the in-
tersection of the posterior border of the tongue
and the inferior border of the mandible to the clos-
est point on the posterior pharyngeal wall.67
MP may result from pituitary adenoma with
acromegaly.66 Pituitary adenomas are benign tu-
mors located in the sella turcica and usually asso-
ciated with hypersecretion of pituitary hormones.
One of these hormones is growth hormone (GH).
The GH-secreting pituitary adenoma leads to acro-
megaly, which is a highly disproportionate growth
of the mandible and facial bones in postpubertal
patients, mainly as a result of reactivation of the
subcondylar growth zones and also due to perio-
steal bone apposition.66
Patients with cleft lip–cleft palate clearly exhibitt
the underlying potential for midfacial deficiencyy
or skeletal Class III growth as a result of the
J Formos Med Assoc | 2006 • Vol 105 • No 10

original deformity and subsequent multiple ope-
rations necessary for its repair.64 Cleft cases with
midfacial deficiency usually underdevelop antero-
posteriorly and also vertically, leading the accen-
tuation of the relative mandibular protrusion in
maxillary retrognathism or MP.64
Dentofacial Orthopedic Therapy in
Growing Class III Children
Treatment of MP or skeletal Class III malocclu-
sion in growing children remains one of the most
challenging problems confronting the practicing
orthodontist. A number of treatment protocols
have been used to address skeletal Class III cases,
including the chincup,9,19,20 face mask,70–73 max-
illary protraction combined with chincup trac-
tion74,75 and the Fränkel functional regulator III
appliance.76,77
The chincup is recommended in growing pa-
tients who have a moderately protrusive mandible
and a relatively normal anteroposterior position
and maxilla size.78 While chincup therapy for MP
has been used for a long time, varying levels of
success have been reported. Differences in these
findings may be causally related to the duration
of treatment, level of force utilized in the appli-
ance and/or the age of the patient being treated.
This orthopedic appliance is effective for mandi-
bular prognathic patients in late deciduous or early
mixed dentition.78 After resolution of the inter-
maxillary skeletal imbalance, both the amount
of chincup force and the duration of wear are
reduced. The appliance is then used as a retainer
for the remainder of the treatment period.
Maxillary protraction is recommended for devel-
oping skeletal Class III patients with maxillary
deficiency. For a growing patient who suffers
from maxillary retrognathia with or without mild
MP, maxillary protraction with a face mask is an
adequate treatment method. Maxillary protrac-
tion therapy is sometimes combined with palatal
expansion in the belief that palatal expansion
may disrupt the circummaxillary suture system
and thus enhance the protraction effect of the
J Formos Med Assoc | 2006 • Vol 105 • No 10
Treatment off mandibular prognathism
face mask.70,71 However, controlled prospective
randomized clinical trials by Turley71,79 and
Vaughn et al80 demonstrated that maxillary pro-
traction therapy with or without palatal expansion
produced equivalent changes in the dentofacial
complex that combined to improve the skeletal
and dental Class III correction. Their results sug-
gest that the indication for palatal expansion
should be based on clinical criteria (such as
maxillary constriction or space deficiency) otherr
than assisting the Class III correction.
Appliances that combine maxillary protraction
and chincup traction are appropriate for skeletal
Class III patients showing both midface deficiencyy
and moderate MP.75 Combining maxillary pro-
traction therapy for the midface deficiency with
the necessary mandibular retraction strategy often
produces satisfactory results. Skeletal Class III pa-
tients with midface deficiency and MP are often
less difficult to treat than patients with MP alone,
since some improvement may be obtained in the
midface by maxillary protraction, and some in
the mandible by chincup therapy.81 They may nott
respond as well if the strategies are focused on
one region only.
The ultimate treatment goal for skeletal Class
III patients should not only be the correction off
the jaw relationship and negative incisal overjett
related to mesial occlusion at that stage, but also
the stabilization of the intermaxillary skeletal and
dental relationships resulting from orthopedicc
appliance treatment. Thus, close observation and
follow-up of midfacial and mandibular growth
during adolescence, particularly during the sec-
ond or third stage of orthodontic treatment, are
essential.
Using dried human skulls with strain gauges,
Omatsu and Kawamoto82 investigated the effects
of a chincup on the pediatric craniofacial skeleton.
This included consideration of different direc-
tions of traction force imparted by the chincup.
They found that when the direction of traction was
20° more vertical than the chin–condyle line, i.e.
through the occlusal surfaces of the molars, the
vertical-pull chincup (VPCC) produced strong ver-
tical compression stress on the maxillary molars,
785
H.P. Chang, et al
suggestive of induction of counterclockwise rota-
tion of the mandible. Therefore, this treatment
strategy may prevent the relapse of treated ske-
letal Class III malocclusion. The effects of ortho-
pedic force produced by VPCC were correlated
with the cephalometric and histologic observa-
tions during use of this appliance in animal
studies.83,84
Orthognathic Surgery Combined with
Orthodontic Therapy in Adult MP
Facial growth modification can be an effective
method of resolving skeletal Class III jaw discre-
pancies with dentofacial orthopedic appliances.
Nevertheless, continued growth in early adulthood
may detract from treatment results obtained in
childhood or adolescence. Orthognathic surgery in
conjunction with orthodontic treatment would be
required for correction of this problem in adults.85
Skeletal Class III patients make up a consider-
able percentage of the orthognathic surgery popu-
lation. A number of surgical techniques can be
used for the treatment of maxillofacial deformities.
According to the location of the sagittal jaw
problem in adult skeletal Class III cases, orthog-
nathic surgical treatment is accomplished by a
mandibular setback, a maxillary advancement or
a combination of the two. Several methods have
been proposed for surgical correction of MP. The
two most commonly applied surgical procedures
to correct MP are sagittal split ramus osteotomy
(SSRO)86,87 and intraoral vertical ramus osteo-
tomy.88–90 Both are suitable for patients in whom
a desirable occlusal relationship can be obtained
with setback of the mandible, each having its
own advantages.
Dentoalveolar compensation is characteristic
of skeletal Class III malocclusion. In prognathic
patients, dentoalveolar compensation is com-
mon in both maxillary and mandibular arches.
Prognathic patients compensate for the inter-
maxillary skeletal dysplasia during mandibular
protrusion by lingual tipping of the mandibular
incisors with alveolar process. The lower incisors
786
and alveolar retroinclination may result from a
restraining effect of the orbicularis oris muscula-
ture on the crowns as the roots are carried for-
ward by the prognathic mandible.4 In contrast, the
upper incisors and upper alveolar process in prog-
nathic adults are more proclined compared with
normal controls. The upper incisors with alveolarr
process may be tipped labially by the tongue while
the mandible is prognathic.4 Such compensatoryy
dentoalveolar changes should be eliminated from
both arches during orthodontic treatment presur-
gically or postsurgically.91 Orthodontic prepara-
tion can eliminate dentoalveolar compensations
by aligning the teeth over the basal bone to allow w
maximal repositioning of the mandible.
The diagnosis and planning of treatment forr
patients with these maxillofacial deformities can
be complex and challenging. It is important to
determine the quantity of necessary surgical cor-
rection of the prognathic mandible and/or retro-
gnathic midface. This will allow design of the
desired correction possible by an orthodontic pre-
paration. Considering the needs of each patient,
the therapeutic goal is to eliminate dentoalveo-
lar compensation. An orthodontic preparation
with dentoalveolar decompensation will allow an
increase in the quantity of surgical correction,
making better functional and aesthetic results
possible.
Relapse after maxillofacial surgery for the cor-
rection of jaw deformities is distressing to both
clinicians and patients. The muscular factor is re-
garded as being most important in postoperative
relapse following mandibular setback.92 The mostt
reliable fixation method to reduce postoperative
relapse is rigid fixation because it provides stabil-
ity of the postoperative position and reduces re-
lapse.93,94 The other consideration is to reduce
muscular force, since postoperative relapse could
be exacerbated by tension in the pterygomassetericc
sling95 or by postoperative contracture of the oper-
ated soft tissue and muscles.96 Additional methods
for preventing postoperative relapse were consid-
ered with glossectomy and condylar positioning.
In Class III cases, when the condyles are displaced
inferoanteriorly, the condyles tend to return into
J Formos Med Assoc | 2006 • Vol 105 • No 10

the fossa, which thereby reduces the likelihood
of postoperative relapse.97,98
Rigid fixation has been recognized as a success-
ful method for preventing relapse, although apply-
ing the distal ostectomy technique (intentional
ostectomy of the posterior part of the distal seg-
ment) in addition to bilateral SSRO is even more
effective as it offers even better long-term posi-
tional stability.98 This may be due to the reduction
of tension in the pterygomasseteric sling that
applies force in the posterior mandible.
For the practicing orthodontist and oral max-
illofacial surgeon, modern molecular techniques
may appear to be of little relevance. However,
MP and cleft lip–cleft palate have a genetic back-
ground. It is important for clinicians to be well
informed of the molecular background of these
conditions, such as distraction osteogenesis and
bone grafting.
Conclusion
Further research into the growth changes and/or
treatment effects of the VPCC with the direction
of traction through the occlusal surfaces of maxil-
lary and mandibular molars85 on a large number
of patients with skeletal Class III malocclusion is
needed.
Newer techniques of patient management such
as distraction osteogenesis of the maxillary com-
plex and orthodontic implant therapy99 require
rigorous investigation and assessment. Therapies
that are targeted at regional dysmorphoses may
produce a more stable posttreatment outcome.
One good example is distraction osteogenesis,
which, as a mainstay in bone engineering, has
significantly improved reconstructive maxillofacial
procedures. However, the molecular mechanisms
governing the formation of new bone in the inter-
segmental gap of gradually distracted bone seg-
ments remain largely unclear. It has been recently
implicated that a growing number of cytokines
(i.e. growth factors) are intimately involved in the
regulation of bone synthesis and turnover. The
gene regulation of these numerous cytokines
J Formos Med Assoc | 2006 • Vol 105 • No 10
Treatment off mandibular prognathism
during distraction osteogenesis has yet to be
characterized. This will ultimately guide the devel-
opment of targeted strategies designed to acceler-
ate bone healing.
Future work will employ molecular genetics
to identify candidate genes within the human
genome to predict those individuals most likelyy
to develop MP. Further studies in molecular biol-
ogy are needed to disclose the gene–environmentt
interactions associated with the phenotypic di-
versity of MP and the heterogenic developmental
mechanisms thought to be responsible for them.
Identification of candidate genes will permit earlyy
clinical diagnosis and intervention, as the growingg
craniofacial complex may be amenable to prophy-
lactic treatments. Identification of the susceptible
genes in the linkage regions will pave the way forr
insights into the molecular pathways that cause
MP, especially overgrowth of the mandible, and
may lead to the development of novel therapeuticc
tools.
References
1. Angle EH. Treatment of Malocclusion of the Teeth and
Fractures of the Maxillae, 6th edition. Philadelphia: SS
White Dental Mfg Co, 1900.
2. Lischer BE. Principles and Methods of Orthodontia.
Philadelphia: Lea & Febiger, 1912.
3. Susami R, Asai Y, Hirose K, et al. The prevalence of maloc-
clusion in Japanese school children. J Jpn Orthod Soc 1972;
31:319–24. [In Japanese]
4. Chang HP. Components of Class III malocclusion in
Taiwanese. Kaohsiung J Med Sci 1985;1:144–55. [In
Chinese]
5. Kang HK, Ryu YK. A study on the prevalence of malocclu-
sion of Yonsei University students in 1991. Korean J Orthod
1992;22:691–701. [In Korean]
6. Tang EL. The prevalence of malocclusion amongst Hong
Kong male dental students. Br J Orthod 1994;21:57–63.
7. Thilander B, Myberg N. The prevalence of malocclusion
in Swedish school children. Scand J Dent Res 1973;81:
12–20.
8. Jacobson A, Evans WG, Preston CB, et al. Mandibular
prognathism. Am J Orthod 1974;66:140–71.
9. Graber LW. Chin cup therapy for mandibular prognathism.
Am J Orthod 1977;72:23–41.
10. Kameda A. The Begg technique in Japan. Am J Orthod
1982;81:209–27.
787
H.P. Chang, et al
11. Yang WS. The study on the orthodontic patients who
visited Department of Orthodontics, Seoul National
University Hospital. J Korean Dent Assoc 1990;28:
811–21. [In Korean]
12. Nartallo-Turley P, Turley PK. Cephalometric effects of com-
bined palatal expansion and facemask therapy on Class III
malocclusion. Angle Orthod 1998;68:217–24.
13. Susami R. A cephalometric study of dentofacial growth in
Class III subjects with anterior crossbite. J Jpn Orthod Soc
1967;26:1–34. [In Japanese]
14. Chang HP, Kinoshita Z, Kawamoto T. Craniofacial pattern
of Class III deciduous dentition. Angle Orthod 1992;62:
139–44.
15. Chang HP, Lin HC, Liu PH, et al. Midfacial and mandibular
morphometry of children with Class II and Class III mal-
occlusions. J Oral Rehabil 2005;32:642–7.
16. Liu PH, Chang CH, Chang HP. Investigation of midfacial
and mandibular morphology: strain tensor analysis. J Chin
Inst Eng 2003;26:771–80.
17. Fischer-Brandies H, Fischer-Brandies E, Acevedo AI. Ceph-
alometric evaluation of skeletal mandibular prognathism.
Int J Orthod 1985;23:4–8.
18. Chang HP, Lin HC, Liu PH, et al. Craniofacial morphometric
analysis of mandibular prognathism. J Oral Rehabil 2006;
33:183–9.
19. Chang HF, Chang HP, Liu PH, et al. Thin-plate spline graphi-
cal analysis of the mandible in mandibular prognathism.
J Formos Med Assoc 2002;101:790–4.
20. Chang HP, Liu PH, Chang HF, et al. Thin-plate spline (TPS)
graphical analysis of the mandible on cephalometric radio-
graphs. Dentomaxillofac Radiol 2002;31:137–41.
21. Chang HP, Hsieh SH, Tseng YC, et al. Cranial base morpho-
logy in children with Class III malocclusion. Kaohsiung
J Med Sci 2005;21:159–65.
22. Ford HE. The growth of the foetal skull. J Anat 1956;90:
63–72.
23. Diewert VM. A morphometric analysis of craniofacial
growth and changes in spatial relations during secondary
palatal development in human embryos and fetuses. Am
J Anat 1983;167:495–522.
24. Burdi AR, Lawton TJ, Grosslight J. Prenatal pattern emer-
gence in early human facial development. Cleft Palate
J 1988;25:8–15.
25. Lewis AB, Roche AF. The saddle angle: constancy or
change? Angle Orthod 1977;47:46–54.
26. Lestrel PE, Roche AF. Cranial base shape variation with
age: a longitudinal study of shape using Fourier analysis.
Hum Biol 1986;58:527–40.
27. Kerr WJ. A method of superimposing serial lateral cephalo-
metric films for the purpose of comparison: a preliminary
report. Br J Orthod 1978;5:51–3.
28. Bhatia SN, Leighton BC. A Manual of Facial Growth.
Oxford: Oxford University Press, 1993.
29. Burdi AR. Cephalometric growth analysis of the human
upper face region during the last two trimesters of gesta-
tion. Am J Anat 1969;125:133–42.
788
30. Diewert VM. Growth movements during prenatal develop-
ment of human facial morphology. In: Dixon AD, Samat BG,
eds. Normal and Abnormal Bone Growth: Basic and
Clinical Research. New York: Alan R. Liss, 1985:57–66.
31. Diewert VM, Shiota K. Morphological observations in
normal primary palate and cleft lip embryos in the Kyoto
collection. Teratology 1990;41:663–77.
32. Scott JH. The cranial base. Am J Phys Anthropol 1958;16:
319–48.
33. Scott JH. Dento-facial Development and Growth. Oxford:
Pergamon Press, 1967.
34. Dibbets JM. Morphological associations between the
Angle classes. Eur J Orthod 1996;18:111–8.
35. Anderson D, Popovich F. Relation of cranial base flexure to
cranial form and mandibular position. Am J Phys Anthropol
1983;61:181–8.
36. Williams S, Andersen CE. The morphology of the poten-
tial Class III skeletal pattern in the growing child. Am J
Orthod 1986;89:302–11.
37. Kerr WJ, Adams CP. Cranial base and jaw relationship. Am
J Phys Anthropol 1988;77:213–20.
38. Lestrel P, Bodt A, Swindler DR. Longitudinal study of cranial
base shape changes in Macaca nemestrina. Am J Phys
Anthropol 1993;91:117–8.
39. Dhopatkar A, Bhatia S, Rocke P. An investigation into the
relationship between the cranial base angle and malocclu-
sion. Angle Orthod 2002;72:456–63.
40. Ellis E, McNamara JA Jr. Components of adult Class III mal-
occlusion. J Oral Maxillofac Surg 1984;42:295–305.
41. Chang HP, Liu PH, Chang CH. Morphogenetic basis for
Class III malocclusion in Asians. J Dent Res 2003;82(Spec
Iss B):2324.
42. Yamaguchi B. Facial flatness measurements of the Ainu and
Japanese crania. Bull Natl Sci Mus Tokyo 1973;16:161–71.
43. Dodo Y. A study of the facial flatness in several cranial series
from East Asia and North America. J Anthropol Soc Nippon
1986;94:81–93.
44. Ishida H. Flatness of facial skeletons in Siberian and other
circum-Pacific populations. Z Morphol Anthropol 1992;79:
53–67.
45. Oka T, Kawamoto T. Craniofacial patterns of Japanese adults
with various types of malocclusion: a counterpart analysis.
J Osaka Dent Univ 1994;28:1–16.
46. Chang HP, Huang HH. Craniofacial pattern of young adults
with various types of malocclusion. Kaohsiung J Med Sci
1998;14:168–76.
47. Iwaki H. Hereditary influence of malocclusion. Am J Orthod
Oral Surg 1938;24:328–36.
48. Stiles KA, Luke JE. The inheritance of malocclusion due to
mandibular proganthism. J Hered 1953;44:241–5.
49. Kraus BS, Wise WJ, Frie RA. Heredity and the craniofacial
complex. Am J Orthod 1959;45:172–217.
50. Schulze C, Wiese W. On the heredity of prognathism.
Fortschr Kieferorthop 1965;26:213–29. [In German]
51. Suzuki S. Studies on the so-called reverse occlusion. J Nihon
Univ Sch Dent 1961;3:51–8.
J Formos Med Assoc | 2006 • Vol 105 • No 10

52. Litton SF, Ackermann LV, Isaacson RJ, et al. A genetic study
of Class III malocclusion. Am J Orthod 1970;58:565–77.
53. Lundström A. Tooth Size and Occlusion in Twins.
Stockholm: A.B. Fahlcrantz Boktryckeri, 1948.
54. Schulze C. On prognathism in twins. Stoma 1965;18:
250–66. [In German]
55. Downs WG. Studies in the causes of dental anomalies.
J Dent Res 1928;8:367–79.
56. Keeler CE. Heredity in dentistry. Dent Cosmos 1935;77:
1147–63.
57. Wolff G, Wienker TF, Sander H. On the genetics of mandi-
bular prognathism: analysis of large European noble fami-
lies. J Med Genet 1993;30:112–6.
58. El-Gheriani AA, Maher BS, El-Gheriani AS, et al. Segrega-
tion analysis of mandibular prognathism in Libya. J Dent Res
2003;82:523–7.
59. Rubbrecht O. A study of the heredity of the anomalies of
the jaws. Am J Orthod Oral Surg 1939;25:751–79.
60. Hodge GP. A medical history of the Spanish Habsburgs—as
traced in portraits. JAMA 1977;238:1169–74.
61. Susami R, Kushida S, Onishi K, et al. Clinical information
of mandibular prognathism cases. J Jpn Orthod Soc 1968;
27:118–24. [In Japanese]
62. Yamaguchi T, Park SB, Narita A, et al. Genome-wide linkage
analysis of mandibular prognathism in Korean and Japanese
patients. J Dent Res 2005;84:255–9.
63. Pascoe JJ, Hayward JR, Costich ER. Mandibular progna-
thism: its etiology and a classification. J Oral Surg 1960;
18:21–4.
64. Chang HP, Chuang MC, Yang YH, et al. Maxillofacial growth
in children with unilateral cleft lip and palate following sec-
ondary alveolar bone grafting: an interim evaluation. Plast
Reconstr Surg 2005;115:687–95.
65. Gold JK. A new approach to the treatment of mandibular
prognathism. Am J Orthod 1949;35:893–912.
66. Chang HP, Tseng YC, Chou TM. An enlarged sella turcica
on cephalometric radiograph. Dentomaxillofac Radiol 2005;
34:308–12.
67. McNamara JA Jr. A method of cephalometric evaluation.
Am J Orthod 1984;86:449–69.
68. Monteleone L, Duvigneaud JD. Prognathism. J Oral Surg
1963;21:190–5.
69. Schoenwetter RF. A possible relationship between certain
malocclusions and difficult or instrument deliveries. Angle
Orthod 1974;44:336–40.
70. McNamara JA Jr. An orthopedic approach to the treatment
of Class III malocclusion in young patients. J Clin Orthod
1987;21:598–608.
71. Turley PK. Orthopedic correction of Class III malocclusion
with palatal expansion and custom protraction headgear.
J Clin Orthod 1988;22:314–25.
72. Chang HF, Tsai CW, Chang HP, et al. Skeletal changes in
patients with maxillary deficiency following face-mask ther-
apy with or without a palatal expander. Chin Dent J 2004;
3:15–27. [In Chinese]
J Formos Med Assoc | 2006 • Vol 105 • No 10
Treatment off mandibular prognathism
73. Chang ZC, Chang HP, Chen YJ, et al. The treatment effects
of the face mask therapy in the midfacial configurations
in skeletal Class III growing patients by means of mor-
phometric techniques. J Formos Med Assoc 2005;104:
935–41.
74. Kettle MA, Burnapp DR. Occipito-mental anchorage in
orthodontic treatment of dental deformities due to cleft lip
and palate. Br Dent J 1955;99:11–4.
75. Chang HP, Lin HC, Liu PH, et al. Geometric morphometric
assessment of treatment effects of maxillary protraction
combined with chin cup appliance on the maxillofacial com-
plex. J Oral Rehabil 2005;32:720–28.
76. Fränkel R. Maxillary retrusion in Class III and treatment
with the functional corrector III. Trans Eur Orthod Soc 1970;
46:249–59.
77. Fränkel R, Fränkel C. Orofacial orthopedics with the func-
tional regulator. Munich: S. Karger, 1989.
78. Deguchi T, McNamara JA Jr. Craniofacial adaptations in-
duced by chincup therapy in Class III patients. Am J Orthod
Dentofacial Orthop 1999;115:175–82.
79. Turley PK. Managing the developing Class III malocclusion
with palatal expansion and facemask therapy. Am J Orthod
Dentofacial Orthop 2002;122:349–52.
80. Vaughn GA, Mason B, Moon HB, et al. The effects of maxil-
lary protraction therapy with or without rapid palatal expan-
sion: a prospective, randomized clinical trial. Am J Orthod
Dentofacial Orthop 2005;128:299–309.
81. Moyers RE. Handbook of Orthodontics, 4th edition.
Chicago: Year Book Publishers, 1988:432–71.
82. Omatsu M, Kawamoto T. Strain distribution in the cran-
iofacial complex of dried human skulls with use off
the chin cup. J Osaka Odontol Soc 1996;59:75–89. [In
Japanese]
83. Shimozuma K. Effects of external vertical forces on the
dentofacial complex of Macaca irus. J Jpn Orthod Soc 1982;
41:413–49.
84. Kanematsu S. Dentofacial changes produced by extraoral
posterior force on the mandible of Macaca irus. J Jpn
Orthod Soc 1988;47:1–36.
85. Bell WH, Hall HD, White RP Jr, et al. Mandibular excess. In:
Bell WH, Proffit WR, White RP Jr, eds. Surgical Correction off
Dentofacial Deformities. Philadelphia: WB Saunders, 1980:
844–1013.
86. Costa F, Robiony M, Politi M. Stability of sagittal split ramus
osteotomy used to correct Class III malocclusion: review
of the literature. Int J Adult Orthodon Orthognath Surg
2001;16:121–9.
87. Trauner R, Obwegeser H. The surgical correction of man-
dibular prognathism and retrognathia and consideration
of genioplasty: surgical procedures to correct mandibular
prognathism and reshaping the chin. Oral Surg Oral Med
Oral Pathol 1957;10:677–92.
88. Ghali GE, Sikes JW Jr. Intraoral vertical ramus osteotomy as
the preferred treatment for mandibular prognathism. J Oral
Maxillofac Surg 2000;58:313–5.
789
H.P. Chang, et al
89. Wilbanks JL. Correction of mandibular prognathism by dou-
ble oblique intraoral osteotomy. A new technique. Oral
Surg Oral Med Oral Pathol 1971;31:321–7.
90. Herbert JM, Kent JN, Hinds EC. Correction of prognathism
by an intraoral vertical subcondylar osteotomy. J Oral Surg
1970;28:651–3.
91. Capelozza Filho L, Martins A, Mazzotini R, et al. Effects of
dental decompensation on the surgical treatment of man-
dibular prognathism. Int J Adult Orthod Orthognath Surg
1996;11:165–80.
92. Rodriguez RR, Gonzalez M. Skeletal stability after mandibu-
lar setback surgery. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 1996;81:31–3.
93. Souyris F. Sagittal splitting and bicortical screw fixation of
the ascending ramus. J Maxillofac Surg 1978;6:198–203.
94. Paulus GW, Steinhauser EW. A comparative study of wire
osteosynthesis versus bone screws in the treatment of
mandibular prognathism. Oral Surg Oral Med Oral Pathol
1982;43:2–6.
790
95. Rowe NL. The aetiology, clinical features and treatment off
mandibular deformity. Br Dent J 1960;108:41–64.
96. Reitzik M. Skeletal and dental changes after surgical cor-
rection of mandibular prognathism. J Oral Surg 1980;38:
109–16.
97. Epker BN, Fish LC. Mandibular prognathism. In: Epker BN,
Fish LC, eds. Dentofacial Deformities, Integrated Ortho-
dontic and Surgical Correction, Volume I. St Louis: CV
Mosby 1986:449–50.
98. Kim MJ, Kim SG, Park YW. Positional stability following
intentional posterior ostectomy of the distal segment in
bilateral sagittal split ramus osteotomy for correction off
mandibular prognathism. J Craniomaxillofac Surg 2002;30:
35–40.
99. Chang HP. Combined Distraction Osteogenesis, Orthodon-
tic, Prosthodontic and Implant Therapy in Multidisciplinary
Patients. New horizons of orthodontics: Annual Meeting
of the Taiwan Association of Orthodontists, December
17–18, 2005.
J Formos Med Assoc | 2006 • Vol 105 • No 10