This document provides information on various benign bone tumors and non-neoplastic bone lesions. It discusses the classification, presentation, diagnostic evaluation and treatment of conditions such as nonossifying fibroma, fibrous dysplasia, osteofibrous dysplasia, lipoma, hemangioma, Paget's disease, and bone infarcts. For many of these asymptomatic lesions, treatment is not required. Symptomatic lesions may be treated with splinting, curettage, bone grafting or internal fixation depending on the severity and location. Recurrence rates after treatment vary between conditions.
2. A benign tumor is a mass of cells that lacks
the ability to invade neighboring tissue
or metastasize.
They mostly occur within the first three
decades of life.
The precise incidence is not known because
many benign lesions are not biopsied.
They outnumber malignant tumors by at
least several hundredfold.
Timely, accurate diagnosis allows
appropriate treatment so that the patients
can not only survive, but also maintain
optimal function of the affected body parts.
3. Mostly classified according to the normal cell
or tissue of origin.
Lesions that do not have normal tissue
counterparts are grouped according to their
distinct clinicopathologic features.
Overall, matrix-producing and fibrous tumors
are the most common.
Among the benign tumors, osteochondroma
and fibrous cortical defect are most frequent.
4. Bone-forming tumors:
Osteoid osteoma
Bone island
Cartilage lesions:
Chondroma
Osteochondroma
Fibrous lesions:
Nonossifying fibroma
Cortical desmoid
Benign fibrous histiocytoma
Fibrous dysplasia
Osteofibrous dysplasia
Desmoplastic fibroma
Cystic lesions:
Unicameral bone cyst
Aneurysmal bone cyst
Intraosseous ganglion cyst
Epidermoid cyst
Fatty tumors:
Lipoma
Vascular tumors:
Hemangioma
Other Nonneoplastic lesions:
Paget disease
“Brown tumor” hyperparathyroidism
Bone infarct
Osteomyelitis
Stress fracture
5. Clinically, present in various ways.
The more common benign lesions are
frequently asymptomatic and are detected as
incidental findings.
Many tumors, however, produce pain or
noticed as a slow-growing mass.
Sometimes, the first hint of a tumor's
presence is a sudden pathologic fracture.
6. Radiographic analysis plays an important role
in diagnosing bone tumors.
Exact location and extent of the tumor.
It can detect features that help limit the
differential diagnosis and give clues to the
aggressiveness of the tumor.
Ultimately, in most instances, biopsy and
histological study are necessary.
8. • Nonossifying fibroma (fibrous cortical defects) is
a common developmental abnormality due to
proliferation of fibrous tissue.
• 35 % of Children
• Mostly asymptomatic and an incidental finding
with or without a fracture.
• Approximately 5% of all investigated benign bone
tumors.
• Primarily in first 2 decades . Boys > Girls.
• Generally, these latent lesions occur in the
metaphyseal region of long bones ;
• 40% in distal femur,
• 40% in proximal tibia,
• 10% in fibula.
9. • A well-defined lobulated
solitary lesion located
eccentrically in the
metaphysis.
• Multilocular appearance
or ridges in the bony wall,
sclerotic borders, erosion
of the cortex.
• There is no periosteal
reaction.
• May occur as a multifocal
lesion.
• The radiographic
appearance is always
typical, and no additional
imaging and biopsy is
warranted
10. • Spindle-shaped cells
distributed in a
whorled pattern.
• There is fibroblastic
proliferation with high
cellularity.
• Giant cells and foam
cells are almost always
apparent.
• Usually no bone
formation
13. Mostly asymptomatic and regress
spontaneously in adulthood.
Most pathological fractures can be treated
conservatively.
Curettage and bone grafting for lesions that
significantly cause weakening the bone.
Large symptomatic lesions, subjected to
repeated trauma require treatment with
Internal fixation & bone grafting.
Recurrence after treatment is rare.
14. • A benign disorder characterized by tumor-like
proliferation of fibro-osseus tissue.
• A developmental abnormality of bone.
• The hallmark is replacement of normal bone and
marrow by fibrous tissue and small, woven
spicules of bone.
• Occur in the epiphysis, metaphysis, or diaphysis.
• Latent, active and aggressive features.
• Occurs in younger age .
• M:F =1:1and 15% of all benign bone tumors.
• Mutations of the Gs alpha gene leading to over
activity of adenylyl cyclase have been identified in
patients.
15. • Three clinical presentations exist:
Monostotic fibrous dysplasia 70%
Polyostotic fibrous dysplasia 25%
McCune-Albright syndrome 2-5%
• McCune-Albright syndrome refers to
polyostotic fibrous dysplasia, cutaneous
pigmentation, and endocrine abnormalities.
16.
17. Pain with complete pathologic fracture or micro-fracture
Swelling with pathologic fracture.
Commonly presents as a long lesion in a long bone.
The ipsilateral proximal femur is invariably affected,
especially proximal femur-varus deformity (Shepherd's crook
deformity) affects hip motion, especially abduction, may
result in limp.
Limb length discrepancy.
Associated abnormalities, such as sexual precocity, abnormal
skin pigmentation, intramuscular myxoma, and thyroid
disease, may be present.
18. • Appearance is characteristic,
witch is lucent purely lytic
having a granular, ground-
glass appearance.
May also contain cystic parts,
calcifications and ossifications.
Thinning of the cortex and
endosteal scalloping.
Bone expansion and bone
deformity (shepherd's crook•
deformity ) involving one end
to the other.
Tiny trabeculae are noted
within the lesion.
19.
20. Variably cellular fibrous
tissue containing irregularly
shaped trabeculae of woven
bone
Woven bone is immature
bone that has not
undergone remodelling into
lamellar bone.
Fibroblasts, with few
mitoses.
Bone appears to arise
directly from fibrous tissue,
not from osteoblasts;
termed "Chinese characters"
because of unusual shape.
24. • Therapy determined by patient's age, activity
of lesion, extent of fracture risk, and mechanical
deformity
• Conservative therapy:
Bracing and modification of activity.
Treatment with bisphosphonates is beneficial
for patients with extensive disease.
25. • Surgical treatment :
Indicated when significant deformity or
pathological fracture occurs or significant
pain exists.
• Symptomatic lesions can be treated by
closed methods (splinting), curettage and
bone grafting, internal fixation, and wide
excision .
• Actual and impending pathological
fractures are best treated with
intramedullary fixation when possible.
26. • Because recurrence rates
are high after curettage
and bone grafting,
cortical bone grafts are
preferred over cancellous
grafts (or bone graft
substitutes) because of
their slower resorption.
• Deformities are corrected
by osteotomy with
internal fixation.
27. Pathologic fracture
Progressive deformity in weight-bearing bones.
Painful stress fractures in femoral neck
Although dysplastic bone heals at normal rate after
fracture, resulting callus also dysplastic and
disease persists.
Transform to sarcoma (most commonly
osteosarcoma, fibrosarcoma of bone)
Third most common cause of osteosarcoma arising
in diseased bone after Paget's and radiation-
induced osteosarcoma
28. Malignant degeneration is rare,0.5% to 1%.
When malignant degeneration occurs, it is usually
in fibrous dysplasia that has received irradiation.
Do not irradiate the bone lesions of fibrous
dysplasia.
29. • Osteofibrous dysplasia (ossifying fibroma of long
bones, also known as Campanacci disease) is a
rare lesion usually affecting the tibia and fibula.
• Patients usually are in the first two decades of
life.
• The middle third of the tibia is the most
frequently affected location.
• Usually diaphyseal, it may encroach on the
metaphysis.
• Pain usually is absent, unless pathological
fracture has occurred.
30. • RADIOLOGY:
• The radiographs show
eccentric intracortical
osteolysis with expansion of
the cortex.
HISTOLOGY:
• Loose fibrous tissue in the
center of the lesion and a
band of bony trabeculae
rimmed by active osteoblasts
at the periphery.
• The lesion must be
distinguished from
monostotic fibrous dysplasia
31. The natural course is unpredictable.
Some lesions regress spontaneously during
childhood; most progress during childhood, but
not after puberty.
Recurrence rates are high after curettage or
marginal resection in children.
Conversely, recurrence rates are low after surgery
in skeletally mature patients.
Pathological fractures can be treated
nonoperatively.
Surgical management is aimed at preventing or
correcting deformity.
33. Intraosseous lipoma is a relatively rare lesion, in
contrast to its soft-tissue counterpart.
The true incidence is unknown because most are
asymptomatic and never come to medical
attention.
Most intraosseous lipomas are discovered as
incidental findings.
34. • The radiographic appearance varies, usually
appear as well-defined lucencies possibly
with a thin rim of reactive bone.
• CT and MRI show well-defined lesions with
the same signal characteristics as fat.
• Central necrosis or calcification sometimes is
evident.
• Biopsy rarely is necessary because imaging
usually is diagnostic.
35.
36. Surgery is indicated only for the rare
symptomatic lesion. In these cases, simple
curettage usually is curative.
38. Hemangioma is a common benign bone lesion.
It is estimated that 10% of the population has
asymptomatic lesions of the vertebral bodies.
Common in the skull & vertebrae, relatively
uncommon in long bones of the extremities.
Discovered as incidental findings.
Spinal lesions rarely are symptomatic unless
there is vertebral collapse or, in rare cases with
soft-tissue extension, nerve root or cord
compression.
39. RADIOLOGY:
Appearance in the spine
usually is characteristic,
with thickened, vertically
oriented trabeculae giving
the classic “jailhouse”
appearance.
On CT Scan cross section,
these thickened trabeculae
have a “polka dot” pattern.
On MRI, the lesions usually
are bright on T1- and T2-
weighted images.
HISTOLOGY:
Rarely needed, reveals a
proliferation of normal-
appearing blood vessels.
40.
41. • Usually is not necessary; however, multiple options
exist for symptomatic lesions.
• Nerve root or cord decompression with spinal
stabilization for rare cases of vertebral collapse
with neurological compromise.
• Most lesions of the long bones can be treated
adequately with extended curettage.
• Preoperative embolization minimize intraoperative
blood loss, which otherwise could be massive.
• Selective arterial embolization can be used as
definitive treatment in surgically inaccessible
locations.
• Low-dose radiation is an option for inoperable
lesions but carries the risk of malignant
degeneration.
43. Paget’s disease of bone is a localized disorder of
bone remodeling, characterized by enhanced
resorption of bone by giant multinucleated
osteoclasts followed by formation of disorganised
woven bone by osteoblasts.
The resultant bone is expanded, weak and
vascular, causing bone pain brittleness and
deformity.
Paget’s disease is a disorder of uncertain origin.
This disease can occur any where but is most
common in the pelvis, skull, the hip and the bones
of the legs.
44. Paget disease may affect 4% of people of
Anglo-Saxon descent who are older than age
55 years, but it is rare in most other
populations.
It is a disorder of unregulated bone turnover.
Excessive osteoclastic resorption is followed
by increased osteoblastic activity.
An early lytic phase is followed by excessive
bone production with cortical and trabecular
thickening.
45. • Radiographic findings
depend on the stage of
the disease.
• In the lytic phase, bone
resorption can take on
a “blade of grass” or
“flame” appearance
beginning at the end of
the bone and
extending toward the
diaphysis.
• Later the radiographs
show bony sclerosis,
thickened cortices, and
thickened trabeculae .
• Bone scans usually are
“hot”.
46.
47. MRI is helpful in this
circumstance because
the marrow signal in
patients with Paget
disease usually
remains normal.
Histology usually
reveals a characteristic
“mosaic” pattern with
widened lamellae,
irregular cement lines,
and fibrovascular
connective tissue.
48. Medical Management :
Consists of nonsteroidal anti inflammatory
drugs, calcitonin, or bisphosphonates.
Serum alkaline phosphatase levels and urine
pyridinium cross-links can be used to monitor the
activity of the disease.
Surgical Management :
Consists of correcting deformity and treating
pathological fractures.
During periods of active disease, intraoperative
bleeding from affected bones can be massive.
49. Approximately 1% of patients with Paget
disease develop a secondary bone sarcoma,
usually an osteosarcoma.
This risk is probably higher for patients with
polyostotic disease.
50. A bony lesion that arises in settings of
excess osteoclastic activity, as hyperparathyroidism.
Primary hyperparathyroidism usually is caused by an
adenoma of the parathyroid glands.
Secondary hyperparathyroidism can occur in patients
with chronic renal failure.
When the disease is discovered early, the skeletal
change usually is limited to diffuse demineralization.
May occur in any bone, most frequently centrally in the
diaphysis.
Only rarely does the change become markedly focal and
produce a “brown tumor” which resembles a giant cell
tumor and is difficult to distinguish from it.
51. BLOOD CHEMISTRY:
The diagnosis should be established by
◦ Serum calcium,
◦ Phosphorus,
◦ Alkaline phosphatase,
◦ Parathyroid hormone levels
MICROSCOPY:
Some microscopic features in hyperparathyroidism,
(1) the giant cells are a little smaller, often
occurring in a nodular arrangement, especially
around areas of hemorrhage;
(2) the stromal cells are more spindle-shaped and
delicate
52. • Intense osteoclastic
and osteoblastic
activity associated with
peritrabecular fibrosis.
• Diffuse subperiosteal
resorption or
generalized
demineralization.
53. More extreme focal bone
resorption may resembles a
primary bone tumor or
metastatic lesion.
Borders are sharp on plain
radiographs, though non-
sclerotic.
May be confused with giant
cell tumor when located in
the epi-metaphysis.
54. Patients with hyperparathyroidism usually are
treated by an endocrinologist. Orthopaedic
management consists of treating actual or
impending pathological fractures
55. Bone infarct refers to ischemic death of the cellular
elements of the bone and marrow.
Idiopathic or secondary to other conditions like
steroid use, alcoholism, sickle cell anemia.
Bone infarct refers to lesions occurring in the
metaphysis and diaphysis of bone.
They also can occur in patients with no other
apparent underlying disorder.
56. The diagnosis usually by plain radiographs.
Bone infarcts usually are well-defined
metaphyseal lesions with irregular borders.
The periphery of the lesion is calcified, in
contrast to chondroid lesions, which are usually
calcified throughout.
Biopsy (usually unnecessary) shows
mineralization of necrotic marrow elements.
Bone scan
CT Scan
MRI
57.
58. TREATMENT:
Bone infarcts usually are asymptomatic, and no
treatment is required. If a patient presents with
pain, another etiology should be sought.
Rarely, malignancy, such as a malignant fibrous
histiocytoma, can occur at the site of a bone
infarct.