J Oral Maxillofac Surg

71:47-52, 2013

Primary Jaw Tumors in Children

Shelly Abramowicz, DMD, MPH,* Batya R. Goldwaser, DMD,†
Maria J. Troulis, DDS, MSc,‡ Bonnie L. Padwa, DMD, MD,§ and
Leonard B. Kaban, DMD, MD储

Purpose: To document tumor type, biological/clinical behavior, management, and outcomes in chil-
dren with primary jaw tumors.
Materials and Methods: A retrospective analysis of children with primary benign jaw tumors evalu-
ated at Massachusetts General Hospital and Children’s Hospital Boston from 1991 to 2009 was con-
ducted. Patients were included if they were aged 16 years or younger and had adequate records and
follow-up. Patient charts, radiographs, and pathology reports were reviewed. Demographic data; clinical,
radiographic, and histopathologic findings; treatment; and outcomes were recorded. Predictor variables
were tumor type, clinical behavior (nonaggressive/aggressive), and treatment. Outcome variables in-
cluded presence or absence of recurrence and complications. Descriptive statistics were computed.
Results: There were 102 patients (44 male and 58 female patients) with a mean age of 8.3 years (range,
6 months to 16 years). Tumors were grouped by tumor type: mesenchymal (n ⫽ 96), neurogenic (n ⫽
5), vascular (n ⫽ 5), or hematopoietic (n ⫽ 3); in addition, when appropriate, they were classified as
nonaggressive (n ⫽ 54) or aggressive (n ⫽ 27). Treatment was based on the tumor’s clinical/biological
behavior and radiographic features and whether it was solitary or multifocal. Patients with nonaggressive
tumors were treated by enucleation, debulking/contouring, or observation, and the recurrence rate was
0%. Aggressive tumors underwent en bloc resection or enucleation with systemic adjuvant therapy, and
the recurrence rate was 7.1%. Mean follow-up was 2.4 years.
Conclusions: The results of this study indicate that primary jaw tumors in children exhibit variable
biological/clinical behavior, often not predicted by descriptive histologic findings. Management of these
tumors should therefore be guided by clinical/biological behavior.
© 2013 American Association of Oral and Maxillofacial Surgeons
J Oral Maxillofac Surg 71:47-52, 2013

Primary benign jaw tumors in children are uncom- with diagnostic and treatment guidelines. They con-
mon, and few surgeons have extensive experience cluded that the benign histologic appearance does
with their management.1 Chuong and Kaban,1 in not predict the aggressive nature of some primary jaw
1985, first reported a series of pediatric jaw tumors tumors. They recommended that management be

*Instructor, Department of Oral and Maxillofacial Surgery, Har-
vard School of Dental Medicine, Boston, MA, and Attending Sur-
geon, Department of Plastic and Oral Surgery, Children’s Hospital
Boston, Boston, MA.
†Resident, Department of Oral and Maxillofacial Surgery, Harvard
School of Dental Medicine, Massachusetts General Hospital, Boston, MA.
‡Associate Professor, Department of Oral and Maxillofacial Sur-
gery, Harvard School of Dental Medicine, Boston, MA, and Resi-
dency Program Director and Visiting Surgeon, Massachusetts Gen-
eral Hospital, Boston, MA.
§Associate Professor, Department of Oral and Maxillofacial Sur-
gery, Harvard School of Dental Medicine, Boston, MA, and Oral
Surgeon-in-Chief, Department of Plastic and Oral Surgery, Chil-
dren’s Hospital Boston, Boston, MA.
储Walter C. Guralnick Professor of Oral and Maxillofacial Surgery,
Harvard School of Dental Medicine, Boston, MA, and Chair, Depart-
ment of Oral and Maxillofacial Surgery, Massachusetts General
Hospital, Boston, MA.
Presented at the 92nd Annual Meeting of the American Associ-
ation of Oral and Maxillofacial Surgeons, Chicago, IL, September
27–October 2, 2010.
Supported in part by Oral and Maxillofacial Surgery Foundation/
American Association of Oral and Maxillofacial Surgeons Faculty
Educator Development Award (S.A.), Massachusetts General Hos-
pital Oral and Maxillofacial Surgery Education and Research Fund
(B.R.G.), and the Hanson Foundation (Boston, MA) (M.J.T.).
Conflict of Interest Disclosures: None of the authors reported
any disclosures.
Address correspondence and reprint requests to Dr Abramo-
wicz: Department of Plastic and Oral Surgery, Children’s Hospital
Boston, 300 Longwood Ave, Boston, MA 02445; e-mail: shelly
.abramowicz@childrens.harvard.edu
© 2013 American Association of Oral and Maxillofacial Surgeons
0278-2391/13/7101-0$36.00/0
http://dx.doi.org/10.1016/j.joms.2012.04.045

47
48
based on biological behavior and not on a descriptive
histologic diagnosis.
The existing literature pertaining to pediatric be-
nign jaw tumors is primarily composed of case re-
ports and small cohort studies. Multiple treatment
modalities have been tried in a variety of lesions. The
inconsistent outcomes reported provide little helpful
guidance for the treating surgeon. In addition, the
reported follow-up periods are inadequate to accu-
rately assess recurrence rates and outcomes.2-5
The aims of this study were to document tumor
type, biological/clinical behavior, management, and
outcomes for children with primary benign jaw tu-
mors.
Materials and Methods
This was a retrospective review of children who
presented to the Oral and Maxillofacial Surgery Ser-
vice at Massachusetts General Hospital (Institutional
Review Board 2009-P002715) or Children’s Hospital
Boston (Institutional Review Board M09-01-00298)
from January 1991 to December 2009. Patients were
included if they 1) had a primary tumor of the maxilla
and/or mandible, 2) were aged 16 years or younger at
the time of presentation, 3) had adequate documen-
tation in hospital and outpatient records, and 4) had
postoperative follow-up of at least 12 months. Pa-
tients with salivary gland or odontogenic tumors; exo-
stoses; enostoses; secondary jaw involvement by tu-
mors of the face, neck, or upper airway; malignant
tumors; insufficient follow-up; or inadequate records
were excluded.
Inpatient and outpatient medical records, radio-
graphs (plain films and computed tomograms), and
pathology reports were reviewed. We documented
the following: age at presentation; gender; race
(white, African American, Hispanic, or other races);
duration of follow-up (interval from first postoper-
ative day to most recent visit); tumor location (max-
illa, mandible, or both); tissue of origin (mesenchy-
mal, neurogenic, vascular, or hematopoietic); rate
of growth (ie, rapid change noted by family vs
asymptomatic/incidental finding); clinical presenta-
tion (swelling, discoloration, bleeding, paresthesia,
pain or tenderness, jaw asymmetry, trauma, delayed
tooth eruption, tooth mobility, or tooth displace-
ment); radiographic findings (size of lesion as mea-
sured on computed tomography, tooth and/or root
displacement, root resorption, cortical thinning or
perforation, or bony expansion); and details of
management (observation, debulking/contouring,
enucleation only, enucleation plus systemic adju-
vant therapy, or en bloc resection).
The outcome variables were cure or recurrence
and complications of treatment. Incomplete treat-
PRIMARY JAW TUMORS IN CHILDREN
ment of a primary lesion was distinguished from true
recurrence. The data were collected using a standard-
ized collection form.
DEFINITION OF AGGRESSIVE LESION
The conceptual framework for management of pri-
mary jaw tumors in children, as advocated by Chuong
and Kaban,1 includes classifying the lesions into non-
aggressive, intermediate, and aggressive categories
based on clinical/biological behavior and radio-
graphic criteria.
The classification was initially described by Chuong
et al6 for use in the management of giant cell lesions
(GCLs) and was later modified.7-9 A tumor was desig-
nated as nonaggressive if it was asymptomatic and
incidentally discovered on a routine radiograph
and/or if it did not meet criteria for an aggressive
tumor.9 Aggressive tumors were defined as those exhib-
iting size greater than 5 cm, rapid growth, or recurrence
after treatment. Radiographic criteria were cortical bone
thinning or perforation, tooth displacement, and root
resorption. Tumors with at least 3 of the previously
mentioned criteria were classified as aggressive.9 If
multifocal or bilateral tumors are present, hyperpara-
thyroidism, cherubism, and Noonan syndrome should
be ruled out.10,11
Fibro-osseous lesions (FOLs) include ossifying fi-
broma and fibrous dysplasia. Ossifying fibroma usually
occurs as a single tumor, whereas fibrous dysplasia
may be monostotic, multifocal/polyostotic, or polyo-
stotic with café au lait spots and multiple endocrine
abnormalities (McCune-Albright syndrome). For pur-
poses of classification, FOLs are divided into quies-
cent/stable, slow growing, and aggressive/rapidly
growing.12 Quiescent lesions are often asymptomatic
and exhibit no active growth. Radiographically, they
appear radiopaque. Slow-growing FOLs may become
quite large but generally do not produce pain, pares-
thesia, or functional impairment. Radiographically,
they exhibit a ground-glass or radiopaque appearance
with interspersed radiolucent areas. Aggressive FOLs
typically grow rapidly to a large size and appear as
multilocular radiolucencies with tooth displacement
and cortical thinning or perforation. They may cause
functional problems, such as airway obstruction, loss
of vision/hearing, pain, or pathologic fractures.12-15
Myxofibroid lesions include myxoma/fibromyx-
oma, myofibroma, and desmoplastic fibroma/aggres-
sive fibromatosis. The incidence of these tumors is
low; there are few reports of diagnosis and treatment
in the literature. In general, nonaggressive myxofi-
broid lesions are asymptomatic and are usually inci-
dentally discovered during radiographic examination.
Aggressive myxofibroid lesions grow rapidly, infiltrate
between teeth, and exhibit radiographic cortical thin-
ning or perforation and tooth displacement.13,16,17
ABRAMOWICZ ET AL
Results
There were 197 children with benign jaw tumors
evaluated during the study period. Of these patients,
95 did not meet the inclusion criteria and were ex-
cluded, leaving 102 patients (44 male and 58 female
patients) with a mean age of 8.3 years (range, 6
months to 16 years) for analysis. The majority of
patients were white (n ⫽ 86); the remaining patients
were Hispanic (n ⫽ 5), African American (n ⫽ 2), and
other races (n ⫽ 9). There were 109 tumors in the
102 patients; these involved the mandible in 69 pa-
tients (63.3%), the maxilla in 26 (23.9%), or both jaws
in 7 (12.8%). The tissue of origin was mesenchymal in
96 tumors, neurogenic in 5, vascular in 5, and hema-
topoietic in 3. Because the majority of tumors in this
series were mesenchymal in origin, we concentrated
the analysis on this group.
The mesenchymal tumors included GCLs (n ⫽ 45),
FOLs (n ⫽ 30), and myxofibroid lesions (n ⫽ 14). The
GCLs were categorized as nonaggressive (n ⫽ 23),
aggressive (n ⫽ 12), or part of cherubism (n ⫽ 3) or
Noonan syndrome (n ⫽ 2). The FOLs included fibrous
dysplasia (n ⫽ 14), ossifying fibroma (n ⫽ 12), and
osteoblastoma (n ⫽ 4). The FOLs were quiescent/
stable (n ⫽ 13), slow growing (n ⫽ 10), or aggressive/
rapidly growing (n ⫽ 7). The most common myxofi-
broid tumor was myofibroma (n ⫽ 12); 1 patient had
desmoplastic fibroma, and 1 patient had fibromyx-
oma.
When we classified mesenchymal tumors based on
clinical/biological behavior, nonaggressive lesions
(n ⫽ 54) had a mean size of 3.8 cm (range, 1 to 6 cm)
whereas aggressive lesions (n ⫽ 27) were a mean of
5.1 cm (range, 2 to 10 cm). The difference in tumor
size between these groups was statistically significant
(P ⬍ .001). Aggressive tumors commonly caused dis-
coloration of the overlying soft tissue (n ⫽ 11), pain
and tenderness (n ⫽ 10), jaw asymmetry (n ⫽ 8),
tooth mobility (n ⫽ 8), tooth displacement (n ⫽ 7),
jaw fracture (n ⫽ 5), delayed tooth eruption (n ⫽ 3),
bleeding (n ⫽ 3), paresthesia (n ⫽ 3), and surface
ulceration (n ⫽ 1). Radiographic findings in aggres-
sive tumors included tooth and/or root displacement
(n ⫽ 30), root resorption (n ⫽ 8), cortical thinning
(n ⫽ 21) or perforation (n ⫽ 19), bony expansion (n ⫽
14), and/or periosteal reaction (n ⫽ 3).
Treatment was based on the tumor’s clinical and
biological behavior and whether it was solitary (n ⫽
91) or multifocal (n ⫽ 5). Nonaggressive GCLs (n ⫽
23) were enucleated and did not recur. Aggressive
GCLs (n ⫽ 12) were managed by en bloc resection
(n ⫽ 4) or enucleation with systemic interferon (IFN)
alfa (n ⫽ 8). Patients who could not tolerate IFN (n ⫽
2) (brachial plexus palsy and acute psychotic epi-
sode) received zoledronate. The mean duration of
49
follow-up for aggressive GCLs was 2.4 years (range, 1
to 16 years). During that period, 1 patient with an
aggressive GCL had a recurrence that occurred after
en bloc resection and was the index case for the
IFN-alfa adjuvant therapy protocol.18 Patients treated
for GCLs with no recurrence at 24 months (n ⫽ 30)
were considered cured.
Quiescent/stable FOLs were contoured (n ⫽ 6) or
enucleated (n ⫽ 4), or observed with no intervention
(n ⫽ 3). Slow-growing FOLs were debulked/con-
toured (n ⫽ 10). Aggressive FOLs were debulked/
contoured (n ⫽ 3), or patients had adjuvant therapy
with IFN and/or pamidronate (n ⫽ 4). Although the
systemic disease (McCune-Albright syndrome) was
controlled in these patients, they had multiple de-
bulking/contouring procedures for esthetic/func-
tional purposes. The mean duration of follow-up for
the FOL group was 3.5 years (range, 1 to 10 years).
The most common myxofibroid tumor was myofi-
broma. Asymptomatic, intraosseous myofibromas (n ⫽
8) discovered on routine radiographs were enucleated,
and there were no recurrences. Exophytic myofibromas
(n ⫽ 4), desmoplastic fibroma (n ⫽ 1), and fibromyx-
oma (n ⫽ 1) grew rapidly and led to clinical and radio-
graphic concerns for an aggressive lesion. They were
thus resected. The mean duration of follow-up for all
lesions was 3.7 years (range, 1 to 13 years) with no
recurrence.
Discussion
The aims of this study were to document tumor
type, biological/clinical behavior, management, and
outcomes of treatment for benign jaw tumors in chil-
dren (Table 1). Although vascular, neurogenic, and
hematopoietic tumors were recorded in this sample
for completeness, they were only mentioned to illus-
trate the diversity of pediatric jaw tumors. These
neoplasms were fewer in number, and the natural
histories and management considerations were differ-
ent from those of the primary mesenchymal jaw tu-
mors. Therefore they will be the subject of another
study.
The variable clinical behavior of mesenchymal jaw
tumors cannot be explained by their uniformly “be-
nign” histologic appearance. At present, there are no
reliable molecular biomarkers to predict clinical be-
havior and prognosis. Thus we recommend that treat-
ment strategies to achieve cure and minimize recur-
rence should be guided by clinical and radiographic
findings that reflect biological behavior.
GIANT CELL LESIONS
Nonaggressive GCLs of the jaws predictably re-
spond to enucleation/curettage.6,19 The use of adju-
vant or alternative therapies such as intralesional
50 PRIMARY JAW TUMORS IN CHILDREN

Table 1. SUMMARY OF BEHAVIOR, MANAGEMENT, AND OUTCOMES OF TREATMENT FOR BENIGN JAW TUMORS
IN CHILDREN

Mean
Follow-Up
Tumor Type Biological Behavior N Treatment (Range) (yr) Recurrence

Giant cell (n ⫽ 45) Nonaggressive 23 Enucleation 2.3 (1-16) None

Aggressive 12 En bloc resection 3.2 (1-7) 1*
(n ⫽ 4) or
enucleation plus
systemic therapy
(n ⫽ 8)
Syndromic 5 NA None
Fibro-osseous (n ⫽ 30) Quiescent/stable 13 Contouring/enucleation/ 3.4 (1-10) NA
observation
Slow growing 10 Debulking with or 1.2 (1-4)
without contouring
Aggressive/rapidly growing 7 Debulking with or 2.7 (1-6)
without contouring
plus systemic therapy
Myxofibroid (n ⫽ 14) Nonaggressive 8 Enucleation 3.9 (1-13) None
Aggressive 6 Resection 6.6 (1-8)
Abbreviation: NA, not applicable; N, number of tumors.
*Index case.
Abramowicz et al. Primary Jaw Tumors in Children. J Oral Maxillofac Surg 2013.

steroids20,21 and systemic22,23 or nasal24,25 calcitonin
is unnecessary because patients with nonaggressive
lesions can be predictably cured with curettage/enu-
cleation alone. Consistent with other reports in the
literature, in our study nonaggressive GCLs that were
enucleated did not recur. In contrast, aggressive GCLs
treated by enucleation alone have a recurrence rate
approaching 70%.8 Kaban et al8 proposed that GCLs
are proliferative vascular lesions dependent on angio-
genesis. As such, aggressive GCLs can be treated with
tumor debulking and postoperative antiangiogenic
agents such as IFN-alfa or bisphosphonates. IFN ap-
pears to inhibit osteoclasts and stimulate osteo-
blasts.9,18 Bisphosphonates inhibit formation, activa-
tion, and survival of osteoclasts.26,27 In our cohort of
patients with aggressive GCLs treated with en bloc
resection or enucleation with systemic adjuvant IFN,
there were no recurrences after a mean follow-up of
4.4 years (range, 1 to 10.2 years). In the latest study by
Kaban et al (2007), there were 26 patients (10 pa-
tients aged ⬍12 years) treated by this protocol. Of
these patients, 16 were cured, 6 were in remission,
and 4 were in active treatment. There were no recur-
rences.
Recent advances in diagnostic techniques for GCLs
may help surgeons identify aggressive lesions early.
Susarla and colleagues28,29 reported the usefulness of
a molecular marker to differentiate between nonag-
gressive and aggressive GCLs. A CD34 level equal to
or greater than 2.5% was 16.7 times more likely to be
associated with an aggressive GCL than a nonaggres-
sive lesion. In addition, the availability of adjuvant
pharmacologic therapies has allowed surgeons to
achieve cure rates for aggressive GCLs without en
bloc resection. Currently, we are exploring candidate
molecular markers using gene array technology to
predict the behavior of GCLs. In the future, gene
testing may provide a specific definitive method for
differentiating nonaggressive and aggressive GCLs to
guide treatment.
FIBRO-OSSEOUS LESIONS
Papadaki et al12 divided FOLs into 3 categories for
purposes of treatment guidelines: quiescent/stable;
slow growing; and aggressive/rapidly growing. Quies-
cent/stable or slow-growing FOLs are usually enucle-
ated, observed, or contoured for esthetic purposes.12-15
It should be noted that the majority of FOLs ultimately
become quiescent in late adolescence. Aggressive
FOLs or those with systemic disease are not resect-
able; thus, management consists of debulking/con-
touring with adjuvant pharmacologic therapy such
as bisphosphonates30,31 and/or concomitant treat-
ment of systemic disease.32 In our cohort of pa-
tients with FOLs, quiescent/stable lesions were suc-
cessfully treated by contouring, enucleation, or
observation. Aggressive or systemic FOLs were de-
bulked/contoured with adjuvant therapy and/or
treatment of systemic disease. Mean follow-up was
3.5 years.
Systemic therapies are being developed to treat
disease; intravenous and oral bisphosphonates have
ABRAMOWICZ ET AL
been used to slow disease progression30-32 and to
help with associated pain.30-32 Disease activity can
now be monitored with serum alkaline phosphatase
levels.31 Available gene testing for some FOLs (eg,
GNAS gene for McCune-Albright syndrome) provide
promise for future gene therapy.33
MYXOFIBROID LESIONS
Myxofibroid tumors in children are uncommon.
The small number of published reports has shown
that nonaggressive myxofibroid lesions respond to
enucleation but aggressive lesions require resec-
tion.1,13 Desmoplastic fibroma (osseous counterpart
of soft tissue fibromatosis) and myxomas are known
to extend into surrounding bone and are thus consid-
ered locally aggressive.34,35 Accordingly, in our co-
hort, tumors consistent with diagnosis of desmoplas-
tic fibroma and fibromyxoma were resected. Mean
follow-up was 3.7 years with no recurrence. Clinical and
radiographic examination of myofibromas showed 2
patterns (exophytic and intraosseous). In our study co-
hort, intraosseous lesions were successfully enucleated.
On the basis of the location and infiltrative nature of the
exophytic/aggressive tumors, resection was the only
practical treatment.17 It is possible that in the future, the
increasing knowledge of biology of myxofibroid tumors
may help guide surgical intervention and adjuvant treat-
ment.
LIMITATIONS
There were several limitations of this study. The
low incidence of jaw tumors in children and retro-
spective nature of data collection did not allow for
further statistical analysis. However, despite the small
number of tumors in each group, this represents, in
total, a considerable longitudinal experience and valu-
able lessons.
In conclusion, the results of this study suggest that
treatment of primary jaw tumors should be based on
clinical/biological behavior until consistent and accu-
rate molecular markers are available to predict prog-
nosis and response to therapy. Standard histopatho-
logic descriptive diagnoses frequently do not predict
biological behavior, and both aggressive and nonag-
gressive tumors have similar characteristics. Small,
localized tumors with nonaggressive clinical and ra-
diographic presentation can be enucleated with a
predictable cure rate. Larger, more aggressive tumors
require en bloc resection or enucleation/curettage
with adjuvant pharmacologic therapy. As additional
potential therapeutic targets arise, medical therapy in
combination with enucleation/recontouring may be a
promising strategy for the management of aggressive
jaw tumors in children.
51
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