by the American Association for Laboratory Animal Science
Vol 62, No 2
Cynomolgus macaques (Macaca fascicularis) are small non-
human primates often used in research. Female cynomolgus
macaques have an average weight of 2.5 to 5.7 kg, live for ap-
proximately 37 y in the wild, and typically reach sexual maturity
at approximately 52 mo (4.3 y) of age.25 They are highly adapt-
able social animals that form large groups in which juvenile and
young macaques play frequently with conspecifics of similar age
A 3.0-kg, 2.3-y-old female cynomolgus macaque presented to the
clinic for nonweightbearing in her right leg. She was housed in a
large indoor–outdoor breeding colony that is in compliance with
federal regulations governing the use of animals in research and
with AAALAC guidelines. The macaque was housed and all pro-
cedures were performed under an IACUC-approved protocol. All
examinations of the animal were conducted under sedation with ket-
amine (10 mg/kg IM; Ketamine Hydrochloride Injection, Bioniche
Teoranta, Lake Forest, IL). Routine radiographs taken after physical
examination revealed a transverse fracture through both the tibia
and fibula. Multiple regions of irregular radiographic bone density
with cystic and sclerotic areas were noted in the long bones included
in the radiograph (tibia, fibula, and femur). The fractures occurred at
the sites of some of these irregularities. The macaque was placed in a
cast and put on cage rest. Differential diagnoses at that time included
fibrous dysplasia, osteogenesis imperfecta, bone cysts, osteomyelitis,
Blood work (CBC, complete chemistry) was unremarkable. ALP
levels were within normal limits, as was the calcium:phosphorus
ratio. The macaque tested seronegative for B virus (Cercopithecine
herpesvirus 1), SIV, and simian T-cell leukemia virus and seroposi-
tive for simian retrovirus.
Thirteen days after initial presentation, additional radiographs
were taken of all the long bones (Figure 1), as well as the chest,
abdomen, and skull. Multifocal regions of fairly well-defined,
osteolytic, occasionally expansile lesions with adjacent sclerosis
were present in all long bones: the distal third of the right radius
and ulna; middle third of the left radius and ulna; both distal
humeri; distal half of the left tibia and fibula; proximal and distal
third of the right tibia and fibula; distal half of both femurs; and
both femoral necks, with the right being more severely affected.
No lesions were noted in the skull, ribs, spine, or phalanges. The
fracture sites were healing at a normal pace. The cast was replaced
and the macaque allowed further cage rest.
The radiographs were reviewed by a veterinary radiologist
(AV). There were oval to rounded, cystic, radiolucent regions of
lysis involving the diaphyses and metaphyses of the long bones,
with faint trabecular markings within these lytic zones. These
lytic regions were well-demarcated, had a multilobulated appear-
ance, and were slightly expansile, as evidenced by variable thin-
ning of the cortices and slight widening of the diaphyses at these
sites. Medullary sclerosis of the diaphyses, appearing as multifo-
cal sclerotic and lucent regions, was present. The lesions involved
Polyostotic Fibrous Dysplasia in a Cynomolgus
Macaque (Macaca fascicularis)
Cassondra Bauer,1,* Betty G Dunn,2 Arthur R Brothman,6 Edward J Dick Jr,1
Chris Christensen,7 Andra Voges,4 and Charleen M Moore1,3,5
A 2.3-y-old female cynomolgus macaque (Macaca fascicularis) presented with a broken right tibia and fibula. Radiographs showed
multiple cyst-like defects in all long bones. We suspected that both fractures were pathologic because they occurred through these
defects. Ultrasonography, MRI, and dual X-ray absorptiometry revealed that the defects were filled with soft tissue. Grossly, the
bones were abnormal in shape, and a gelatinous material filled the defects and the surrounding marrow cavity. Histologically,
the gelatinous material was composed of fibrin and cartilage; few normal bone cells were seen. Genetic testing revealed extra
material on the short arm of chromosome 8 in all tissues examined, but no copy number alterations of likely clinical significance
were observed, and no abnormalities were found that were unique to the lesions. In light of the clinical signs and radiographic
and pathologic findings, polyostotic fibrous dysplasia was diagnosed. This report represents the first documented case of fibrous
dysplasia in a cynomolgus macaque.
Received: 12 Sep 2011. Revision requested: 07 Oct 2011. Accepted: 18 Oct 2011.
1Southwest National Primate Research Center, Departments of 2Clinical Laboratory
Sciences and 3Cellular and Structural Biology, University of Texas Health Science Center
at San Antonio, 4Veterinary Imaging Center of South Texas, and 5Department of Genetics,
Texas Biomedical Research Institute, San Antonio, Texas; 6Department of Pediatrics,
Human Genetics, and Pathology and ARUP Laboratories, University of Utah School of
Medicine, Salt Lake City, Utah; 7Veterinary Diagnostic Pathology Service, Joint Pathology
Center, Silver Spring, Maryland.
*Corresponding author. Email: email@example.com
Polyostotic fibrous dysplasia in a cynomolgus macaque
Figure 1. Radiographs of affected Macaca fascicularis at initial presentation. (A) Left arm. (B) Right arm. (C) Left leg. (D) Right leg. (E, F) Pelvis and legs.
Note abnormal lucencies (arrows) in all long bones. A fracture is evident in panels D and F (under the R marker).
Vol 62, No 2
and fibrous osteodystrophy (nutritional hyperparathyroidism),
which was considered unlikely because there was absence of
parathyroid gland hyperplasia. The ovary had scattered mature
follicles and organizing corpora luteum. The final diagnosis was
determined to be polyostotic fibrous dysplasia, in light of the clin-
ical history and radiographic and pathologic findings.
Clonal chromosome aberrations have been reported in human
cases of fibrous dysplasia.5 The immediate lineage of this ma-
caque was known, with the sire, dam, and one male half-sibling
from the same dam being the only directly related individuals.
The dam and half-sibling had no history of abnormalities and
were normal on physical examination. The half-sibling had radio-
graphically normal bones. The sire was unavailable for physical
examination but had no history of abnormalities.
Cytogenetic studies were performed on the affected ma-
caque, dam, and half-sibling. Two aspirates from affected bone
(left radius and left ulna) and a skin sample from the back of
the long bones, with the vertebrae and physes appearing to be
spared. The findings were most consistent with multicentric bone
cysts. Other differential diagnoses included metabolic-type dis-
ease and osteogenesis imperfecta, both of which were considered
unlikely but could not be excluded.
The macaque was checked for healing routinely, with cast
changes approximately every 2 wk. When the fracture was ma-
nipulated, the animal received pain medication (30 mg PO twice
daily; Children’s Motrin Berry Flavor, Johnson and Johnson, New
Brunswick, NJ) for 3 to 8 d as needed based on presentation of
signs associated with pain. When the fracture had healed com-
pletely, the macaque was returned to group housing for observa-
tion. She was placed in a calm, small group of 6 macaques that
were similar to her in age. Bone biopsies were considered but not
completed, because of the fragile nature of her bones and poten-
tial for another fracture.
In group housing, the macaque did well; she was able to loco-
mote and interact normally with her cagemates. Approximately
3 mo later, the macaque again presented because of nonweight-
bearing in her right leg. Physical examination was performed, and
radiographs were taken (Figure 2). A fracture was noted at the
right femoral neck, through the site of a previously noted bony
resorptive lesion. An Ehmer sling was placed, and advanced im-
aging and euthanasia were scheduled. The macaque did well in
the Ehmer sling and began to heal; at no time did she lose weight
or become inappetant. There were no behavioral or physical in-
dicators of pain or distress while the macaque was in the Ehmer
sling. After the second application of the Ehmer sling, the ma-
caque removed the bandage. No sign of pain was present, and be-
cause she was not using her leg, the bandage was not replaced.
On the day of euthanasia, physical examination revealed de-
creased range of motion in the right (fracture-side) hip and knee,
with muscle contracture. All other parameters were within nor-
mal limits. The affected macaque was transported for MRI using
several types of weighted scans (T1, T2, fat-specific). Multiple le-
sions were noted in the long bones. The lesions were not fluid- or
fat-filled but had the same density as soft tissue. A full necropsy
was performed. All diagnostic tests and necropsy were completed
within approximately 3 to 4 h of euthanasia.
At necropsy, each long bone contained both normal and abnor-
mal areas (Figure 3). The bones were distorted at sites concurrent
with the radiographic lesions, usually evidenced by thickening
of the diaphysis and mild bowing. The marrow cavity was filled
with a gelatinous substance, and the cortices were thinner than
normal. The only other abnormal finding was that the right ovary
was enlarged to approximately 5 times normal size and cystic.
Tissue samples were taken for histologic evaluation, fixed in 10%
neutral buffered formalin, decalcified, processed conventionally,
embedded in paraffin, cut at 5 µm, stained with hematoxylin and
eosin, and evaluated by light microscopy by a board-certified vet-
erinary pathologist (EJD). There were similar changes throughout
all the long bones examined. The cortex was generally thin and
blended into a zone of bony trabeculae lined by few osteoblasts
and separated by abundant vascularized fibrous connective tissue
composed of densely packed fibroblasts in a collagen matrix. This
fibroblastic proliferation extended into and filled the marrow cav-
ity. Some sections also contained irregular islands of disorganized
hyaline cartilage either within the areas of fibrosis or uniformly
replacing all the subcortical structures and marrow cavity (Figure 4).
The differential diagnoses included polyostotic fibrous dysplasia
Figure 2. Radiograph taken at second presentation. Note fracture in
right femoral neck.
Polyostotic fibrous dysplasia in a cynomolgus macaque
harvested in 3 d. The skin and bone cyst aspirates were treat-
ed briefly with antimicrobial and antifungal agents and then
placed in culture by using standard explant and collagenase
treatments. The tissues were cultured in Minimal Essential
Medium (Invitrogen, Carlsbad, CA) supplemented with L-
glutamine, FBS, antibiotics, and antimycotics and incubated
the affected animal were obtained and cultured. Heparinized
peripheral blood samples were obtained from the affected ma-
caque, dam, and half-sibling. The blood samples were cultured
in RPMI-1640 supplemented with 15% FBS, 1% L-glutamine,
1% antibiotic–antimycotic solution (Sigma-Aldrich, Atlanta,
GA), 1.5% concanavalin A, and 1.5% pokeweed mitogen and
Figure 3. Long bones from (A through C) the affected monkey and (D through F) an age-matched control. (A) Right femur of affected macaque. Note
the swelling and loss of normal cortical contour (femoral head proximal to fracture site not included). (B) Right tibia and fibula of affected macaque.
Note the swelling and bowing at the initial fracture site. (C) Cross-sections through the right femur of the affected macaque. Note the swollen area with
abnormal (gelatinous) marrow cavity and other relatively normal bone. (D) Right femur of control animal. (E) Right tibia and fibula of control animal.
(F) Cross-sections through right femur of control macaque.
Vol 62, No 2
brous dysplasia plus an endocrinopathy (often precocious pu-
berty) or cutaneous hyperpigmentation (café au lait spots) or
both.1,4,7,10,14,15,17,23 It is difficult to determine whether the cynomol-
gus macaque presented here was hyperpigmented, given that
their skin is more pigmented naturally than that of humans, mak-
ing the differentiation of café au lait spots difficult. Despite the
macaque’s young age, she did have an active ovary with evidence
of ovulation, but whether she had begun functional estrus cycles
is unknown, making it unclear whether she exhibited precocious
Fibrous dysplasia can present with varied severity and often
goes undiagnosed unless a complication, such as a fracture, aris-
es. Pathologic fractures of weight-bearing limb bones are the pri-
mary cause of morbidity, with the 2 sites most commonly affected
being the femur and the skull base.1,15 Fibrous dysplasia is most
commonly diagnosed in young patients, with the first symptom
appearing before the age of 15 y in 80% of known human cases.4
Most lesions are detected by the age of 30.7,10,28 Some literature
reports that the peak fracture rate is within the first decade of
life.7,12,14,15 As patients complete puberty, lesions usually stop pro-
gressing and remain stable.9,21
Radiographically, fibrous dysplasia can present with a number
of different appearances. The most common radiographic finding
is a ‘ground-glass’ appearance.1,7,9,15,28 In the polyostotic form, the
long weight-bearing bones often exhibit bowing due to weakness
and microstress fractures over time.21 Lesions in long bones often
present with a well-defined sclerotic border (‘ring sign’).10 The le-
sions usually are contained within the medullary canal; however,
they can arise in both cancellous and cortical bone, leading to de-
formation of the bone.7 An important differential to consider is os-
sifying fibroma, which can present clinically similarly, but is more
aggressive in nature. Ossifying fibroma lesions almost always
begin in the cortex,18 unlike fibrous dysplasia. The age at radio-
graphic diagnosis is a predictor of the appearance of lesions and
whether secondary changes are present, such as aneurismal cysts.
MRI can be a useful tool to diagnose aneurismal bone cysts.15 The
lesions in this macaque had a varied presentation, with some cyst-
like lesions, thinning of the cortices, and a ground-glass appear-
at 37 °C in a 5% CO2 environment. Cells were harvested and
G-banded by using a trypsin–Giemsa staining technique. Twenty
well-spread, high-resolution metaphases from each sample were
analyzed. Karyotypes were arranged according to size, following
the nomenclature of Cambefort and colleagues.3 All the cells in
each tissue from the affected animal had 42 chromosomes, the
normal number for macaques. Each cell also had a small amount
of extra chromatin on the tip of the short arm of one chromosome
8 (which is homologous to human chromosome 8) that was not
seen in the dam or half-sibling’s karyotypes.
DNA samples from the affected animal and a sex-mis-
matched normal cynomolgus control were prepared for array
comparative genomic hybridization (Microarray Laboratory,
University of Utah) using the Human Genome CGH Micro-
array 44K platform (amadid 14950; Agilent Technologies,
Santa Clara, CA) according to the manufacturer’s protocols.
The data were analyzed by using CGH Analytics 3.5 software
(Agilent Technologies) using the ADM-2 algorithm. This analy-
sis showed a clear duplication for the entire X chromosome,
which was expected in light of the sex-mismatched control.
The derivative log ratio was 0.56, which was higher than that
routinely seen in clinical studies of human DNA (typically less
than 0.2), but this value was acceptable for this interspecies
comparison, and the data were generally without background
noise. For the autosomes, one small duplication (approxi-
mately 50 kb) was detected on human chromosome 20, which
contains the zinc finger protein 337 gene (ZNF337). No other
abnormal copy number alterations were observed.
Fibrous dysplasia is an uncommon skeletal condition in which
normal bone is replaced with fibro-osseous tissue and has a wide-
ly varied presentation. The term was initially coined by Louis
Lichtenstein in 1938.16 It is a disorder of development, with no
known heritable link4 or sex predisposition.10,28 Lesions can be
found in a single bone (monostotic) or, less often, several bones
(polyostotic), as in the current case. McCune–Albright syndrome
is the most severe form and is characterized by polyostotic fi-
Figure 4. Histologic appearance of long bones from affected monkey. (A) Right femur. Note the thin cortex, decreased trabeculae, and medullary re-
placement by fibrous and cartilaginous tissue. (B) Right fibula. Note the complete replacement of the medullary cavity by cartilage.
Polyostotic fibrous dysplasia in a cynomolgus macaque
Fibrous dysplasia has also been noted to occur in a canine8 and
New advances in knowledge about fibrous dysplasia have
pointed to skeletal stem cell mutations in the imprinted GNAS
gene on chromosome 20q13 that mediates the pathologic cystic
changes in bone.4,7,15,17,24 This mutation leads to abnormal prolifer-
ation and differentiation of bone marrow stromal cells. The stage
of development at which the mutation occurs seemingly dictates
the severity of the signs seen.4,15 The GNAS mutation is likely to be
present in significant numbers only in the affected tissues.15
Comparative studies on baboon and macaque chromosomes
have shown they have virtually identical karyotypes and a
close relationship to the human karyotype,2,20 such that human
DNA probes can be used successfully to identify baboon and
macaque chromosomal abnormalities.19,26 The ZFP337 gene,
which is located within the 50-kb duplication seen in the af-
fected macaque, is a highly conserved gene that is expressed
in multiple tissues across species. This gene does not appear
to be associated with any abnormal phenotype and is included
in a genomic region containing copy number variants (UCSC
Genome Browser, http://genome.ucsc.edu), suggesting that
the duplication found in the affected animal is a normal vari-
ant. In addition, a gain in this region has also been reported in
an otherwise healthy person in the Database of Genomic Vari-
ants (http://projects.tcag.ca/variation/). These data, combined
with the sex chromosome control data, indicate that there were
no copy number alterations of likely clinical significance in the
The finding of clonal chromosome changes in several reports
of fibrous dysplasia indicates that this condition may, at least in
some cases, be neoplastic in nature.5,6,22 Trisomy 2 and structural
12p13 aberrations have been reported as recurring abnormalities.
Although the macaque we report may have had a constitutional
chromosomal variant or hemicryptic translocation, none of the
abnormalities were unique to the lesions.
Technical assistance and animal care was provided by Verla Atkins,
Lauren Brown, and Silverio Pedroza, Southwest National Primate
Research Center, San Antonio, TX. MRI scans were completed by Dr
Peter Kochunov, University of Texas Health Science Center—Research
Imaging Center, San Antonio, TX. We thank Marie Silva, Michaelle
Hohmann, and Denise Trejo for pathology support. We thank Jeff
Rogers, Texas Biomedical Research Institute, for supplying control DNA
and samples and Heidi Whitby for her assistance with the array CGH
1. American Society for Bone and Mineral Research. 2009. Fibrous
dysplasia in primer on the metabolic bone diseases and disorders
of mineral metabolism, ch 89. Hoboken (NJ): John Wiley and Sons.
2. Best RG, Diamond D, Crawford E, Grass FS, Janish C, Lear TL,
Soenksen D, Szalay AA, Moore CM. 1998. Baboon–human homolo-
gies by spectral karyotyping (SKY): a visual comparison. Cytogenet
Cell Genet 82:83–87.
3. Cambefort Y, Mounié C, Colombiès P, Moro F. 1976. Topographies
des bandes chromosomiques chez Papio papio. Ann Genet 19:5–9.
4. Chapurlat RD, Orcel P. 2008. Fibrous dysplasia of bone and McCu-
ne–Albright syndrome. Best Pract Res Clin Rheumatol 22:55–69.
5. Dal Cin P. [Internet]. 2001. Bone: fibrous dysplasia of the bone.
Atlas of genetics and cytogenetics in oncology and haematology.
ance. The lesions seemed to be confined to the medullary canal,
with some distortion of the cortical bone.
Grossly, bones with fibrous dysplasia are described as having
a yellowish discoloration with a gritty feel.7 This manifestation
is due to the disorganized trabeculae within the lesions. On cut
surface, the gross lesions in this macaque were pale tan in color,
with a gelatinous feel. Individual bones contained both grossly
normal and abnormal sections.
Histologically fibrous dysplasia presents with a ‘Chinese char-
acter’ appearance of abnormal disorganized trabecular bone.15
The woven bone is immature, devoid of rimming osteoblasts and
osteoclasts, with spindle cells in a whorled arrangement.10 The
trabeculae show a pattern of disorganized deposits, despite thick-
ness and maturity under polarized light.7,10,23 Normal maturation
of bone follows the pattern of woven bone deposition followed
by rimming of spicules with rows of osteoblasts which then de-
posit bone matrix layers (osteiod). Over time, the woven bone is
replaced by lamellar bone.23 Fibrous dysplasia lesions exhibit no
rimming of trabeculae by osteoblasts and no evidence of lamellar
replacement of woven bone. Ossifying fibroma differs in that the
trabeculae are surrounded by active osteoblasts.13,18,27 In fibrous
dysplasia, often the cortical bone is preserved but is thin,23,28 as
was seen in the current case. Marrow spaces in fibrous dyspla-
sia lesions are filled with cellular tissues arranged in a random
fashion.23 Many human cases have active fibroblasts.21 Histologic
changes due to treatment may complicate obtaining an accurate
Malignancy in fibrous dysplasia is rare, with osteosarcoma
being the most common neoplasm.1,7,10,15,28 Polyostotic forms
of the disease are more likely to develop malignancy than are
monostotic forms.10,28 Other secondary changes include aneu-
rismal bone cysts at the sites of intralesional hemorrhage.10 An-
eurismal bone cysts were a consideration for this macaque and
may have been present as secondary changes due to fibrous
Diagnosis of fibrous dysplasia primarily is based on clinical
findings, radiographic evidence, and histologic findings.4,15
Diagnostic laboratory results may also play a role, with eleva-
tion of markers of bone turnover (ALP, calcium:phosphorus
ratio, and so forth) and the presence of other derangements
from normal (hypophospatemia, phosphaturia, endocrine ab-
normalities). Serum biochemistry results for this macaque were
unremarkable, and a urinalysis was not obtained.
The only treatment available for fibrous dysplasia is to manage
pain and repair fractures. In human medicine, the fractures of-
ten are pinned. Compared with the monostotic form, polyostotic
fibrous dysplasia has a higher risk of deformity and complica-
tions, due the presence of multiple lesions. In addition, bisphos-
phonates to inhibit osteoclasts are used in human medicine, with
some reported success.4,7,15 Because our macaque was bred as part
of a research colony and would be unsuitable for study, she was
euthanized. While diagnostics were being performed, she was
treated with pain medication, and the fractures were treated ac-
Fibrous dysplasia is a rare disorder in humans and appears to
be equally rare in animals. There are only 2 reports of fibrous dys-
plasia in nonhuman primates, both occurring in the maxilla; one
case involved a spider monkey11 and the other a cebus monkey.29
Another reported case of multiple cystic lesions in the bones of a
spider monkey was determined to be Gorham–Stout syndrome.30
Vol 62, No 2 Download full-text
[Cited 02 June 2011]. Available at: http://AtlasGeneticsOncology.
6. Dal Cin P, Sciot R, Brys P, De Wever I, Dorfman H, Fletcher CD,
Jonsson K, Mandahl N, Mertens F, Mitelman F, Rosai J, Rydholm
A, Samson I, Tallini G, Van den Berghe H, Vanni R, Willen H.
2000. Recurrent chromosome aberrations in fibrous dysplasia of the
bone: a report of the CHAMP study group. Cancer Genet Cytogenet
7. DiCaprio MR, Enneking WF. 2005. Fibrous dysplasia. Pathophysiology,
evaluation, and treatment. J Bone Joint Surg Am 87:1848–1864. .
8. DiMeo A, Pepe M, Mechelli L, Spaterna A. 1998. Polyostotic fibrous
dysplasia in a dog. Vet Comp Orthopaed Traumatol 11:112–117.
9. Döhler JR, Hughes SPF. 1986. Fibrous dysplasia of bone and the
Weil–Albright syndrome. Int Orthop 10:53–62.
10. Dorfman HD. 2010. New knowledge of fibro-osseous lesions of
bone. Int J Surg Pathol 18:62S–65S.
11. Duncan JR, Lederer HA, Ramsey FK, Tyler DE. 1962. Fibrous dys-
plasia in a monkey. Iowa State Univ Vet 25:81–82.
12. Hart ES, Kelly MH, Billante B, Chen CC, Ziran N, Lee JS, Feuillan
P, Leet AI, Kushner H, Robey PG, Collins MT. 2007. Onset, progres-
sion, and plateau of skeletal lesions in fibrous dysplasia and the re-
lationship to functional outcome. J Bone Miner Res 22:1468–1474.
13. Herrero FA, Muñoz AS, Rodriguez MM, Sancho FG. 2006. Ossify-
ing fibroma of long bones in adults: a case report. Acta Orthop Belg
14. Leet AI, Chebli C, Kushner H, Chen CC, Kelly MH, Brillante BA,
Robey PG, Bianco P, Wientroub S, Collins MT. 2004. Fracture in-
cidence in polyostotic fibrous dysplasia and the McCune–Albright
syndrome. J Bone Miner Res 19:571–577. .
15. Leet AI, Collins MT. 2007. Current approach to fibrous dysplasia
of bone and McCune–Albright syndrome. J Child Orthop 1:3–17.
16. Lichtenstein L. 1977. Bone tumors, 5th ed, p 409–415. St Louis (MO):
17. Lietman SA, Schwindinger W, Levine M. 2007. Genetic and mo-
lecular aspects of McCune–Albright syndrome. Pediatr Endocrinol
18. Markel SF. 1978. Ossifying fibroma of long bone. Am J Clin Pathol
19. Moore CM, Hubbard GB, Dick E, Dunn BG, Raveendran M,
Rogers J, Williams V, Gomez JJ, Butler SD, Leland MM, Schlabritz-
Loutsevitch NE. 2007. Trisomy 17 in a baboon (Papio hamadryas) with
polydactyly, patent foramen ovale, and pyelectasis. Am J Primatol
20. Moore CM, Janish C, Eddy CA, Hubbard GB, Leland MM,
Rogers J. 1999. Cytogenetic and fertility studies of a rheboon, rhesus
macaque (Macaca mulatta) × baboon (Papio hamadryas) cross: further
support for a single karyotype nomenclature. Am J Phys Anthropol
21. Ozaki T, Sugihara M, Nakatsuka Y, Kawai A, Inoue H. 1996.
Polyostotic fibrous dysplasia a long-term follow-up of 8 patients.
Int Orthop 20:227–232.
22. Parham DM, Bridge JA, Lukacs JL, Ding Y, Tryka AF, Sawyer JR.
2004. Cytogenetic distinction among benign fibro-osseous lesions
of bone in children and adolescents: value of karyotypic findings in
differential diagnosis. Pediatr Dev Pathol 7:148–158.
23. Reed RJ. 1963. Fibrous dysplasia of bone: a review of 25 cases. Arch
24. Riminucci M, Robey RP, Saggio I, Bianco P. 2010. Skeletal progeni-
tors and the GNAS gene: fibrous dysplasia of bone read through stem
cells. J Mol Endocrinol 45:355–364.
25. Rowe N. 1996. The pictorial guide to the living primates. East
Hampton (NY): Pogonias Press.
26. Ruppenthal GC, Moore CM, Best RG, Walker-Gelatt CG, Delio PJ,
Sackett GP. 2004. Trisomy 16 in a pigtailed macaque (M. nemestrina)
with multiple anomalies and developmental delays. Am J Ment
27. Schmelting B, Zöller M, Kaspareit J. 2011. Peripheral ossifying
fibroma and juxtacortical chondrosarcoma in cynomolgus monkeys
(Macaca fascicularis). J Am Assoc Lab Anim Sci 50:98–104.
28. Taconis WK. 1988. Osteosarcoma in fibrous dysplasia. Skeletal Radiol
29. Williamson WM, Lombard LS, Firfer HS. 1965. Fibrous dysplasia
in a monkey and a kudu. J Am Vet Med Assoc 147:1049–1052.
30. Wimsatt J, Withrow SJ, Danner D, Powers B, Hagler T, Pritzker
KPH. 2011. Multicystic bone disease (Gorham–Stout Syndrome) in
a spider monkey (Ateles geoffroyi). J Med Primatol 40:61–70.