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Pathology Patterns Reviews

S50 Am J Clin Pathol 2002;118(Suppl 1):S50-S70

© American Society for Clinical Pathology

A b s t r a c t

Benign fibro-osseous lesions (BFOLs) of the
maxillofacial bones represent a diverse group of
pathologic conditions that includes developmental
lesions, reactive or dysplastic diseases, and neoplasms.
Owing to substantial overlap of the histopathologic
findings, subclassification of BFOLs may be
problematic. Moreover, this is not merely an academic
exercise because the therapeutic management of BFOLs
varies depending on the actual disease process. To
further complicate matters, a number of other disease
processes demonstrate clinical, radiographic, and
microscopic features that bear resemblance to those
encountered in recognized fibro-osseous conditions.
The objective of this article is to review the most current
clinicopathologic, radiographic, and molecular studies
of BFOLs to aid the surgical pathologist in the
recognition and diagnosis of this diverse group of
maxillofacial lesions. A discussion of the various
disease processes that occasionally may be confused
with BFOLs also is included.

Benign fibro-osseous lesions (BFOLs) of the maxillofa-
cial bones comprise a diverse group of pathologic conditions
that includes developmental lesions, reactive or dysplastic
diseases, and neoplasms.1 Regardless of subtype, all BFOLs
demonstrate replacement of normal bone by fibrous connec-
tive tissue with an admixture of mineralized product,
including osteoid, mature bone, and/or cementum-like calcifi-
cations. Thus, a histologic diagnosis of a BFOL is, in many
cases, relatively uncomplicated. The main challenge lies in
the subclassification of BFOLs. Moreover, this is not merely
an academic exercise because the therapeutic management of
BFOLs varies depending on the actual disease process.1

Historically, the nosology of BFOL has been fraught
with inconsistency, confusion, and a seemingly endless array
of terminology.1-6 However, a classification of BFOLs
proposed by Waldron6 has gained wide recognition over the
years and remains, to date, the most accepted. Recently,
Brannon and Fowler1 proposed a slightly modified catego-
rization of BFOLs, which, with further study, eventually may
become the standard ❚ Table 1❚ . Nevertheless, despite
advances in our understanding of these conditions, occasional
lesions still defy classification.6

From a clinical standpoint, BFOLs may be associated
with significant cosmetic and functional disturbances, or they
may be completely asymptomatic, localized lesions that are
identified only on routine radiographs.1,4,5,7 Furthermore,
fibrous dysplasia, a form of BFOL typically diagnosed in
children and adolescents, can be associated with a general-
ized endocrinopathy.2 Moreover, there are pronounced racial
and sex predilections for a subset of BFOLs that exclusively
affects the jawbones, the osseous dysplasias, of which a
hereditary form exists.4 Radiographically, BFOLs may mani-
fest as solitary, multifocal, or multiquadrant disease; they

Benign Fibro-osseous Diseases of the Maxillofacial Bones

A Review and Differential Diagnosis

Faizan Alawi, DDS

Key Words: Benign fibro-osseous lesion; Fibrous dysplasia; Ossifying fibroma; Osseous dysplasia; Cementoma


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Pathology Patterns Reviews

Am J Clin Pathol 2002;118(Suppl 1):S50-S70 S51

© American Society for Clinical Pathology

may be ill or well defined; they may have a radiolucent, mixed
radiolucent-radiopaque, predominantly radiopaque, or ground-
glass appearance; they may be monostotic or polyostotic; and
they may or may not be associated with the root apices of
teeth.7 The gross appearance of BFOLs also may vary
depending on the lesion. Thus, most oral and maxillofacial
pathologists would agree that definitive diagnosis of a BFOL
requires correlation of the histologic appearance of the lesion
with the clinical, radiographic, and intraoperative findings.1,6

The objective of this article is to review the most current
clinicopathologic, radiographic, and molecular studies of
BFOLs to aid the surgical pathologist in the recognition and
diagnosis of this diverse group of maxillofacial lesions. A
number of other disease processes demonstrate clinical, radi-
ographic, and microscopic features that bear resemblance
to those encountered in recognized fibro-osseous condi-
tions.2 Thus, other entities that may be included in the
differential diagnosis of BFOLs also will be discussed
❚ Table 2 ❚ . However, it must be noted that these other
lesions do not completely fulfill the histologic criteria for
BFOLs as defined by Waldron.6 The interested reader is
directed to a number of other articles, including an excellent
review by Brannon and Fowler,1 detailing the historic contro-
versies surrounding the putative pathogenesis, diagnosis, and

classification of BFOLs.2-6 With respect to nomenclature in
the present article, the Brannon and Fowler1 classification
system is used.

True BFOLs

Fibrous Dysplasia

Fibrous dysplasia (FD) is a benign fibro-osseous disease
that frequently affects the jawbones. It has been suggested
that the diagnosis of FD is overused in clinical practice and
should be reserved for only the lesions that manifest as
poorly delineated, expanding lesions in children and young
adults.2,8 FD is classified as being monostotic when it affects
a single bone or, less commonly, polyostotic when it involves
multiple bones concomitantly. About 3% to 5% of polyos-
totic FD may be associated with extraosseous
manifestations.9 McCune-Albright syndrome (MAS) is a
sporadic disorder that is characterized by the clinical triad of
polyostotic FD, skin hyperpigmentation (café au lait spots),
and multiple endocrinopathies, including gonadal hyperfunc-
tion leading to sexual precocity (especially in females).9

Other less common manifestations of MAS include hyper-
thyroidism, adenomas of various endocrine glands including
the pituitary gland, Cushing syndrome, acromegaly, benign
ovarian cysts, linear epidermal nevi, and neonatal
cholestasis.9-13 The skin spots often are unilateral and ipsilat-
eral to the FD lesions.14

Mazabraud syndrome is another rare, sporadic disease
that is characterized primarily by polyostotic FD and intra-
muscular myxomas.15 The myxomas tend to appear many
years after the initial manifestations of FD. There have been
about 40 documented cases of this unusual disorder;
however, there seems to be some clinical overlap with MAS,
since patients with Mazabraud syndrome also may have café
au lait spots, and patients with MAS reportedly have devel-
oped soft tissue myxomas.16,17

Although the exact cell of origin remains unclear, it
seems that FD is derived from osteoprogenitor, fibroblast-
like cells.18,19 It has been determined that monostotic FD,
polyostotic FD, MAS, and sporadic pituitary adenomas have
the same causal genesis, an activating, somatic mutation in
the GNAS1 gene found on chromosome 20q13.9,12,13,20 Two
distinct missense mutations in the alpha subunit of a G stim-
ulatory protein have been identified that seem to account for
most of the aforementioned disease processes.12 The muta-
tions lead to constitutive activation of adenylyl cyclase,
resulting in a persistent elevation of cyclic adenosine
monophosphate. This, in turn, induces an alteration in the
transcription and expression of several downstream target
genes, including c-fos, a proto-oncogene.19,21

❚❚ Table 1❚❚
Recognized Benign Fibro-osseous Diseases*

I. Fibrous dysplasia
A. Monostotic
B. Craniofacial
C. Polyostotic
D. McCune-Albright syndrome

II. Ossifying fibroma and juvenile ossifying fibroma
III. Osseous dysplasia

A. Periapical
B. Focal
C. Florid
D. Familial gigantiform cementoma

* Adapted from the classification system proposed by Brannon and Fowler.1

❚❚ Table 2❚❚
Disease Processes That May Be Included in the Differential
Diagnosis of a Benign Fibro-osseous Lesion

Paget disease of bone
Low-grade osteosarcoma
Osteoid osteoma
Central odontogenic fibroma
Proliferative periostitis
Renal osteodystrophy
Central giant cell granuloma
Brown tumor
Aneurysmal bone cyst

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Pathology Patterns Reviews

radiolucent-radiopaque areas ❚ Image 9❚ .7,32,72 The disease is
limited exclusively to the tooth-bearing areas of the jaws, thus
sparing the inferior cortex and ascending ramus of the mandible.
Both dentulous and edentulous areas may be affected. Anterior
mandibular involvement typically manifests radiographically as
periapical osseous dysplasia, which reinforces the concept that
both florid osseous dysplasia and periapical osseous dysplasia
are part of the same disease spectrum.4 Concomitant multiple
traumatic bone cysts commonly develop in association with
florid osseous dysplasia, manifesting as well-delineated, cyst-
like radiolucencies.6,72 In occasional cases, these cysts may
represent the initial manifestation of florid osseous dysplasia.72

Florid osseous dysplasia is a clinical and radiographic
diagnosis in which at least 2 quadrants must be involved to
make the diagnosis.4 Although a biopsy may be performed for
diagnostic purposes, it usually is unnecessary in asymptomatic
patients and, in most cases, not recommended. This is because
the densely sclerotic, calcified masses are avascular and, thus,
are susceptible to infection if exposed to the oral flora. The
subsequent development of an acute or chronic osteomyelitis
may lead to substantial bone loss, sequestration of the sclerotic
masses, and fistula formation ❚ Image 10❚ .4,72 As a result, in
typical cases, therapeutic management for asymptomatic
patients consists of long-term follow-up, maintenance of excel-
lent oral hygiene, preventive dental care, and elimination of any
inflammatory stimuli that may predispose to infection.1 In
symptomatic patients, treatment often is more challenging and
not always successful.6 Antibiotic therapy and surgical debride-
ment of the infected sclerotic bone usually are necessary. To
date, there has been only 1 documented case of sarcomatous
transformation in a patient with florid osseous dysplasia of the
mandible.73 However, this latter case may represent a coinci-
dental finding since osseous dysplasias do not demonstrate an
appreciable risk for malignant transformation.4

Florid osseous dysplasia–like lesions have been identi-
fied in other disorders. A rare osteogenesis imperfecta–like
syndrome, also termed gnathodiaphyseal dysplasia and
hereditary gnathodiaphyseal sclerosis, has been recog-
nized.74,75 In addition to bone fragility and modeling defects
of the tubular bones, multiple BFOLs involving the tooth-
bearing regions of the jawbones also have been noted.74 Both
the maxilla and mandible typically are involved, and, in the
few cases reported, multiquadrant disease is not unusual.3,74,75

Although not completely characterized, radiographically, the
lesions seem to resemble those seen in florid osseous
dysplasia. Moreover, affected patients seem to have a propen-
sity for jaw infection.74 The microscopic appearance of the
jaw lesions is consistent with that of a BFOL.

Familial Gigantiform Cementoma

Another genetic disorder that is characterized by florid
osseous dysplasia–like lesions of the jawbones also has been

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© American Society for Clinical Pathology

focal osseous dysplasia exhibits little tendency to enlarge
over time; thus, further treatment usually is unneces-
sary.4,70,71 However, periodic, long-term follow-up is recom-
mended, because patients with focal osseous dysplasia may
develop additional lesions in other parts of the jaws, leading
to the suggestion that focal osseous dysplasia may represent
the initial manifestation of florid osseous dysplasia.70

Florid Osseous Dysplasia
Florid osseous dysplasia is the most clinically extensive

form of osseous dysplasia.1 However, florid osseous dysplasia
is, in most cases, an innocuous, self-limiting disease. Like the
other 2 forms of osseous dysplasia, florid osseous dysplasia
arises mainly in black females during the fourth and fifth
decades of life.4,72 However, there are numerous documented
cases of florid osseous dysplasia in Asian females as well.71

Florid osseous dysplasia commonly involves the posterior
regions of the mandible, manifesting as bilateral, relatively
symmetrical lesions. Moreover, simultaneous, bilateral
involvement of both jaws is very common.4,6 In most cases
affected patients are asymptomatic, and the disease is
detected only on routine dental radiographs. However, occa-
sional patients may have dull, intermittent, poorly localized
pain, especially in lesions that are infected secondarily.4,72

Unlike patients with periapical osseous dysplasia and focal
osseous dysplasia, patients with florid osseous dysplasia may
have limited bony expansion, especially of the mandible.4

Radiographs often demonstrate numerous, irregularly
shaped, sclerotic radiopacities admixed with diffuse, ill-defined,

❚ Image 8❚ Focal osseous dysplasia. Periapical radiograph
showing a relatively well-circumscribed radiolucency with a
central nidus of calcification. Note the close association of
the lesion with the root apex of the molar tooth.

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identified. This condition, labeled familial gigantiform
cementoma (FGC) or familial florid osseous dysplasia, is an
autosomal dominant disorder with variable phenotypic
expressivity.76,77 A number of affected families have been
identified, including a large pedigree of 55 individuals span-
ning 3 generations.76 The radiographic appearance is iden-
tical to that of florid osseous dysplasia, ie, multiquadrant,
dense lobular radiopacities with ill-defined radiolucent-
radiopaque areas. Like florid osseous dysplasia, there is no
clinical or radiographic evidence of disease in other parts of
the skeleton. However, unlike florid osseous dysplasia, there
is no sex, age, or racial predilection for FGC.76,77 Lesions
often manifest at an early age and may cause substantial
rapid bony expansion and facial asymmetry.

Sporadic cases of FGC also have been reported with
features analogous to the familial form.78 Moreover, the
clinical features differentiate the sporadic form of FGC
from florid osseous dysplasia. In addition, the clinicoradi-
ographic manifestations of sporadic FGC resemble those
seen in patients with multiple OFs. Thus, it has been
suggested that cases previously reported as “multiple ossi-
fying fibromas” should more appropriately be characterized
as sporadic FGC.78

Based on the clinical manifestations, it seems that FGC
is a benign heritable or sporadic neoplastic process demon-
strating a multifocal growth pattern. Moreover, given the
often synchronous involvement of both jawbones, FGC may
be viewed as a polyostotic benign fibro-osseous disease.78

Owing to the often rapid expansion of the lesions, surgical

intervention usually is necessary. If clinically feasible,
conservative but complete surgical excision is recommended.
Recurrence has been reported.

Lesions That May Resemble BFOLs

A number of neoplastic, nonneoplastic, and metabolic
disease processes may manifest with clinical, radiographic,
and histopathologic features that closely resemble those seen
in BFOLs. However, these diseases do not completely satisfy
the histologic criteria required for a diagnosis of a BFOL, as
outlined by Waldron.6 Nevertheless, owing to the wide array
of lesions that may be included in the differential diagnosis
of a BFOL, an accurate diagnosis may be challenging, espe-
cially when evaluating small, fragmented tissue specimens in
the absence of adequate clinical and radiographic data.

Paget Disease of Bone

Paget disease of bone (PDB) is a chronic, focal disease
of the bones that affects 3% to 5% of the population older
than 40 years.79 Males are more commonly affected than
females and whites more often than blacks. PDB is charac-
terized by excessive bone resorption owing to increased
osteoclastic activity, coupled with rapid, disorganized bone
remodeling.79,80 Although the exact cause remains unclear, a
number of studies have identified a substantial genetic
component, with evidence of linkage to 4 distinct loci.80-82

Furthermore, a familial, autosomal dominant form of PDB

❚ Image 9❚ Florid osseous dysplasia. Panoramic radiograph
demonstrating diffuse, ill-defined, radiolucent-radiopaque
lesions of the mandible, extending bilaterally. Maxillary
involvement was not noted.

❚ Image 10❚ Florid osseous dysplasia with secondary
osteomyelitis. A bony sequestrum is seen extruding through
the overlying alveolar mucosa.

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