emedicine.medscape.

com

eMedicine Specialties > Orthopedic Surgery > Neoplasms

Osteoid Osteoma
Gerard Librodo, MD, Consulting Staff, Flinthills Orthopaedics
Charles T Mehlman, DO, MPH, Professor of Pediatrics and Pediatric Orthopedic Surgery, Division of
Pediatric Orthopedic Surgery, Director, Musculoskeletal Outcomes Research, Cincinnati Children's
Hospital Medical Center
Updated: Apr 23, 2010
Introduction
Background

Osteoid osteoma is a benign osteoblastic tumor that Bergstrand first described in 1930.[1 ]Jaffe described it
in 1935 and was the first to recognize it as a unique entity.[2 ]Osteoid osteomas are usually smaller than 1.5-
2 cm and characterized by an osteoid-rich nidus in a highly loose, vascular connective tissue. The nidus is
well-demarcated and may contain a variable amount of calcification. Surrounding the nidus is a zone of
sclerotic but otherwise normal bone.[3,4,5,6 ]

An image depicting osteoid osteoma can be seen below.

Anteroposterior (AP) and lateral radiographs of osteoid osteoma. Courtesy of Cincinnati Children's
Hospital Medical Center, Department of Pediatric Orthopaedics.

Location of the Lesion

Osteoid osteoma can occur anywhere. It can involve a single bone or several bones. Osteoid osteoma is
reported to occur in the cortex of the shafts of long bones in 80-90% of cases. It is also reported in the
epiphyseal and metaphyseal regions of both small and large bones of the axial and appendicular skeletons,
especially the femur, tibia, and humerus.
Extremities
The lower extremities are the most common sites of osteoid osteomas. The femur, particularly the
intertrochanteric or intracapsular regions of the hip, is affected in two thirds of cases.[7,8 ]The diaphyseal part
of the tibia and the humerus are other common sites. Barei et al reported that in 50-60% of cases, osteoid
osteoma occurs in the femur and tibia.[9,10 ]
Spine
Approximately 7-20% of osteoid osteomas involve the spine. Involvement here most commonly manifests
as painful scoliosis, but painless conditions can also occur. Pettine et al noted that 50% of lesions occur in
the cervical spine, and up to 78% of osteoid osteomas in the lumbar spine are associated with scoliosis.
[11,12,13,14 ]

The tumor has a predilection for the posterior elements, most commonly affecting the cancellous lamina,
spinous process, and pedicle but sparing the vertebral bodies. Wells et al observed this predilection in 75%
of cases, with 33% involving the lamina, 20% involving the articular facets, and 15% involving the
pedicles.[15 ]About 59% of osteoid osteomas affect the lumbar spine. Rates in other areas are 27% in the
cervical spine, 12% in the thoracic spine, and 2% in the sacrum.
Other locations
Other areas that may be involved include the hand, talus, foot, and joints.[16,17,18 ]Osteoid osteomas of the
hand and wrist are rare, most commonly involving the phalanges, and often result in atypical clinical and
radiologic characteristics. The findings are similar to those of tumors involving the foot and ankle. Intra-
articular osteoid osteoma occurs in 10% of cases and can involve the hip, elbow, and ankle.
Frequency
Osteoid osteoma is a relatively common bone tumor, accounting for approximately one eighth to one tenth
of all symptomatic benign bone tumors and 5% of all primary bone tumors.
Age
Osteoid osteoma is generally a condition of the young, but it can affect a wide range of individuals aged 8
months to 70 years. The literature reports that people aged 10-30 years are most susceptible. About 90% of
cases occur in patients younger than 25 years. In fact, Barei et al noted that 70% of osteoid osteomas
occurred in patients younger than 20 years.[9 ]The tumor is less common in patients older than 30 years,
accounting for 13% of cases. About 3% of cases occur in children younger than 5 years.[19,20 ]
Sex
Men are affected more frequently than women. The male-to-female ratio is 2-3:1.
Race
No racial or ethnic predilection is noted for osteoid osteoma.
Differential Diagnoses
Clinical picture
Patients with osteoid osteoma can present with an atypical history and lesions in unusual locations. Because
of this presentation, osteoid osteomas can be confused with osteomyelitis, especially Brodie abscesses,
eosinophilic granulomas, and other benign cysts.
Radiographic appearance
Radiographic findings of osteoid osteoma may mimic those of stress fractures, intracortical abscesses,
sclerosing osteomyelitis of Garré, or avascular necrosis. It should be differentiated from osteochondritis
dissecans and inflammatory arthritis. On rare occasions, it can resemble osteosarcoma.

Features on bone scanning

Histologically, osteoid osteoma is almost identical to osteoblastoma, osteosarcoma, and enostosis.
However, benign osteoblastoma has a uniform pattern of thick, closely packed trabeculae with increased
cellularity and vascularity. Osteosarcoma and parosteal osteosarcoma are more cellular than osteoid
osteoma, and they are anaplastic with elaborate malignant osteoid. Enostosis, on the contrary, represents
the opposite extreme, with islands of densely packed, thickened bone trabeculae with normal stroma.[21 ]
Histologic appearance
Osteoid osteoma can appear as spondylolysis on bone scans; both can appear as abnormal activity in the
spine. Wells et al noted that in cases of spondylolysis, immediate postinjection images showed minimal or
no abnormal activity but that abnormal activity was observed when imaging was delayed after the injection.
[15 ]
Early uptake of tracer is detectable in all cases of osteoid osteoma. Delayed images reveal unilateral or
bilateral abnormalities in cases of spondylolysis but demonstrate intense tracer accumulation in cases of
osteoid osteoma.[22 ]
Natural History
The natural history of osteoid osteoma is controversial. The literature suggests a history of resolving pain
and healing of the lesions, but no histologic confirmation of the diagnosis has been reported. The course of
this disease is unpredictable and protracted, with intervals of resolution of pain that sometimes last 6-15
years.
Atar et al (1992) described 2 stages of the disease.[23 ]The first is an acutely painful stage that lasts 18-36
months, during which patients require steady use of analgesics. The second is the recovery stage, which
includes healing of the nidus and which usually takes 3-7 years. Barei et al noted that healing involves
ossification of the untreated nidus, which cannot be readily distinguished from surrounding bone and which
resembles a localized zone of cortical hypertrophy.[9 ]
Clinical Presentation
Signs and symptoms
Symptoms of osteoid osteoma can last from weeks to years before diagnosis and eventual surgery. Pain is
the principal symptom of both initial and recurrent disease. It is described as a continuous, deep, aching,
and intense pain with varying quality and severity. It is typically localized to the site of the lesion. Pain is
usually worse at night (in 95% of patients) and diminishes by morning. The pain may awaken the patient
(29% of cases). Some patients may have an exertional component, especially those with intracapsular
lesions with synovitis and restricted range of motion. The pain may also affect the patient's gait.
The pain usually occurs before the lesions are visible on radiographs. The pain is responsive to oral
salicylates, often with dramatic beneficial results, but the response is not universal. In approximately 50-
75% of patients, it responds to oral salicylates. Pain symptoms can be exacerbated with the use of ethanol.
Osteoid osteoma should be considered in any young patient with pain in the back or neck, painful scoliosis,
or radicular or referred-type pain into the lower limb or shoulder. Its symptoms can simulate those of a
herniated disk, or the lesion may produce radicular-like symptoms in the shoulders and arms. Unexplained,
rigid, or painful scoliosis, especially if the pain is referred to the concavity of the curve, has been associated
with osteoid osteoma. Local pain is most commonly noted in the area of the tumor.
Swelling can also occur in osteoid osteoma and is sometimes the only presenting symptom. This is usually
observed in patients with diaphyseal lesions.
Osteoid osteoma involving the hand can manifest as monoarticular arthritis,[24 ]macrodactyly, clubbing, and
painless swelling with absence of reactive bone or bony lysis.[25 ]
Physical examination
Physical findings can vary in patients with osteoid osteoma. Tenderness is present in 62% of patients and
usually occurs with subperiosteal lesions; it is relatively uncommon with medullary lesions. Local warmth
and erythema are possible but unusual.
Intracapsular lesions are rare. Epiphyseal lesions mimic intra-articular derangement and can delay the true
diagnosis. These lesions may be associated with proliferative synovitis due to prostaglandin secretion that
decreases range of motion. Joint effusion can be present, mimicking inflammatory arthritis. Soft-tissue
swelling, contractures, and a soft-tissue mass can also be noted. Radiographs may reveal the lack of an
intense perifocal sclerotic margin and perinidal bone marrow edema.
Neurologic findings are variable. Janin et al and MacLellan et al noted a 25% incidence of neurologic
abnormalities.[26,27 ]Reports in the literature describe fewer neurologic abnormalities, such as monoparesis
and paraparesis, with osteoid osteoma than with osteoblastoma because osteoid osteomas are smaller than
osteoblastomas.
Laboratory findings
Patients with osteoid osteoma usually have normal blood and chemistry findings.
Osteoid osteoma has been linked to prostaglandins, which may explain the inflammatory features of the
lesion. Some authors have postulated that prostaglandins may have a fundamental role in the development
of osteoid osteoma.
Several authors have noted extremely high levels of prostaglandin metabolites, especially prostaglandins
E2, I2, and F1 alpha, which have been seen at levels 100-1000 times normal levels, especially in the nidus.
Two pathways have been postulated for pain generation in osteoid osteoma secondary to the effects of
prostaglandin. One pathway involves vasodilatory and permeability effects related to an increase in both
the size of blood vessels and flow in blood vessels in the bony lesion that increases pain and pressure. In
the second pathway, the effects of the bradykinin system potentiate pain akin to that due to injured soft
tissue because of increased capillary permeability.
Diagnostic delay
Delays of 11.8-36 months have been reported in the diagnosis and treatment of osteoid osteoma. Pettine et
al noted that bone scanning dramatically decreased the mean interval from the appearance of symptoms to
diagnosis from 35 months to 12 months.[11 ]
Imaging Studies
Diagnostic Imaging Studies
Radiography
Osteoid osteoma elicits a profound osteoblastic response in surrounding medullary and cortical bone and
shows the characteristic picture of sclerosis around a lucent nidus. It appears as cortical thickening and
diffuse medullary sclerosis on radiographs. Radiography usually reveals a radiolucent area of about 1 cm in
diameter, called the nidus, with a center that is sometimes calcified, resulting in a radiopaque point called
the bell. The nidus is surrounded by a rim or halo of radiodense cortical hypertrophy or hyperostosis.
Cortical lesions may appear with sclerosis that may obscure the lucent nidus.
Intracapsular lesions usually manifest as proliferative synovitis with joint effusion and soft-tissue swelling
and no sclerosis. Atar et al noted that lesions in the femoral neck caused widening and foreshortening of the
femoral neck, with a reduction in the height of the capital femoral epiphysis and with osteoporosis of the
proximal femur.[23 ]
Subperiosteal lesions may not be apparent on plain radiographs.
Epiphyseal and metaphyseal lesions may show only minimal sclerotic changes around the nidus.
Variation in radiographic appearance is possible. Lesions can appear as only a radiolucent zone, only a
radiopaque area, or as a central sclerosis with surrounding radiopacity.
Regarding the diagnostic value of radiography, some authors have reported that the combination of clinical
and radiographic features confirms the diagnosis. However, Georgoulis et al noted that plain radiographs
alone have low diagnostic value in detecting the lesion.[28 ]
Osteoid osteoma may be present months to years before radiographic confirmation. Radiographs may be
normal during the first months after the onset of complaint. Therefore, repeat radiographs should be
obtained from time to time to document osseous manifestations.
Radionuclide scanning
Radionuclide scans are reliable tools when radiographic findings are not diagnostic. Wells et al urged that
bone scans be performed when radiographic findings are normal or inconclusive, especially in pediatric
patients with back pain. Radionuclide concentrates principally in the nidus of osteoid osteoma and
minimally in perifocal bone.[15 ]
Osteoid osteoma is associated with a nonspecific but intense, well-defined uptake of activity on bone scans.
This focus of intense uptake is correlated with the nidus. Meire et al reported the presence of a nonspecific
hot spot long before radiographs depict an alternation of bone texture that represents an osteoblastic lesion.
[29 ]

Technetium bone scanning aids in establishing the diagnosis of osteoid osteoma. Rinsky et al reported that
technetium-99m scintigraphy is sensitive for osteoid osteoma in its early stages.[30 ]In fact, the diagnostic
delay is reduced from 35 months to 12 months with the use of bone scans. Swee et al reported that 25% of
patients with osteoid osteoma presented with negative radiographic findings but positive bone scans.[31 ]
They recommended that bone scanning be done in suspected cases when radiographic findings are normal.
Radionuclide scanning also has the advantage of aiding the surgeon and the pathologist in confirming
resection of the tumor and locating the lesion for histologic examination. Specimen autoradiography and
scintigraphy are accurate in localizing the nidus, thus facilitating histologic examination.[32,33 ]
Bone scintigraphy also is helpful in ruling out multicentric processes.[34,35 ]
To date, no negative bone-scan findings have been reported in patients with osteoid osteoma. Bone
scanning is currently the most accurate means of localizing the tumor. Wells et al noted that the sensitivity
of skeletal scintigraphy for osteoid osteoma is 100%.[15 ]
Osteoid osteoma can sometimes be confused with spondylolysis, especially in the lower lumbar spine, as
both result in a hot spot on bone scans. Wells et al observed 2 basic differences between the diseases.
Images obtained immediately after injection showed minimal or no abnormal activity in spondylolysis. By
comparison, images of osteoid osteoma demonstrated easily detectable uptake of the tracer in all cases.
However, abnormal activity was noted with spondylolysis when a delay occurred between injection and
imaging. On delayed images, both spondylolysis and osteoid osteoma showed hot spots, but spondylolysis
resulted in unilateral or bilateral abnormalities, whereas osteoid osteoma led to intense tracer accumulation.
[15 ]

Arteriography
Arteriography can be used when other examinations fail to give sufficient information. Meire et al
described 3 phases of osteoid osteoma on the basis of arteriographic findings: (1) early arterial phase, (2)
late arterial phase, and (3) venous phase that generates the bluish picture due to the storage of dye.[29 ]
CT scanning
CT is helpful in precisely delineating the nidus. CT scanning is recommended when the nidus is not visible
on conventional radiographs, when residual or recurrent tumor is present, or when the tumor is located in a
critical area (eg, spine or femoral neck). CT increases specificity for calcified lesions and allows for the
visualization of the nidus. It is helpful in precisely defining the location of the tumor and the extent of
osseous involvement, especially in areas deep in complex joints such as the hip.[36,37 ]
CT is more accurate than MRI. Sans et al reported that CT helped in confirming the diagnosis of osteoid
osteoma in 74% of cases.[38 ]Szendroi et al reported accuracies of about 66% in the diagnosis of intra-
articular lesions and 90% in extra-articular lesions.[39 ]To date, CT scanning is the primary investigational
tool for the definitive diagnosis of osteoid osteoma.[40 ]
On CT scans, osteoid osteoma appears as a circumscribed annular lesion with a double-attenuating sign.
When CT is performed with intravenous contrast material, scans of osteoid osteoma typically show a rapid,
early arterial phase of enhancement and then a slow exit of the contrast material from the nidus, consistent
with delayed flow in the venous phase.
Magnetic resonance imaging
A noncalcified nidus has homogeneous enhancement on contrast-enhanced, fat-suppressed T1-weighted
images. By comparison, a calcified nidus has ring enhancement, the intensity of which is proportional to
the extent of the remaining part of the vascularized nidus. On T1-weighted images, the lesion is an area of
decreased signal intensity, sometimes with a bell of highly decreased signal intensity at its center. The
degree of bone marrow and soft-tissue enhancement is directly correlated with the size and reactive
inflammatory changes of the lesion.[41,42,43 ]
MRI has not been useful in the diagnosis of osteoid osteoma. MRI is reserved for equivocal cases because
it can suggest the diagnosis of osteoid osteoma. It is sensitive in detecting bone marrow, peritumoral
edema, and soft-tissue abnormalities. Localization of the nidus is often difficult because of an abundance of
reactive bone and edema surrounding the lesion that is occasionally misleading. Assoun et al noted that
MRI interpretation resulted in notable errors in diagnosis, most often confusion with malignancies.[44 ]
Guzey et al confirmed this finding. They reported that spinal osteoid osteoma with changes on
paravertebral soft tissue can mimic malignant soft-tissue tumors on MRI.[45 ]
The potential rate of missed diagnosis with MRI is 35%. The tumor is identified on only 65% of axial
images. Hence, reliance on MRI alone may lead to clinically significant misdiagnoses. This is particularly
true for medullary lesions.[46 ]
Localization of the Lesion
Preoperative localization
Regardless of the method of treatment, its success highly depends on preprocedural localization of the
nidus. In fact, most authors agree that exact localization of the lesion is the most important determinant of
successful operative removal.
Careful radiographic imaging is necessary to plan surgical treatment. However, radionuclide and CT scans
have been most helpful in localizing the tumor. Radionuclide scans assist in the localization and diagnosis
of osteoid osteoma in its early stages. It is also used in ruling out multicentric processes, which can occur in
osteoid osteoma. On the other hand, CT can assist in preoperative localization, and it is useful in precise
localization of the nidus in the hip or the spine.
Intraoperative localization
Various methods have been used to intraoperatively localize and identify osteoid osteomas to minimize
bone resection and to help ensure complete excision of the tumor.
Klonecke et al reported that intraoperative scanning has evolved because of the excessively wide excision
necessary in the past that had to be planned to help guarantee complete removal of the lesion.[47 ]However,
even with the use of frozen sections, adequate excision is not ensured.
Tetracycline fluorescence under UV light requires patients to take tetracycline before surgery (4 mg per
kilogram of body weight by mouth 4 times a day for 1-2 days). The difficulty of intraoperative
identification of the nidus often leads to nonexcision of the lesion. Information must therefore be obtained
from the excised bone with pathologic examination. If the nidus is not in the specimen, further resection of
the bone is required, resulting in unnecessary and excessive removal of bone.
Intraoperative radiographs can be helpful in localizing the lesion in reference to a guide pin inserted into
the bone. Multiplanar fluoroscopy can help in localizing the nidus if it is in cancellous bone, where
sclerotic reactions are minimal. By comparison, cortical lesions contain reactive sclerosis that may obscure
the nidus, leading to incomplete removal of the lesion and resulting in recurrence.
Rinsky et al first described intraoperative radioisotope scanning for osteoid osteoma.[30 ]Advantages include
intraoperative localization by radionuclide scintillation probe that is easy and reliable, minimizes bone
resection, and does not prolong surgery. It can aid the surgeon and pathologist in confirming resection of
the tumor and in localizing the lesion for histologic examination. It is the only technique that aids in
verifying complete surgical excision of the lesion, with a success rate of 94%. Furthermore, it keeps
procedural morbidity at its lowest level.
CT scanning is helpful for the precise localization of the nidus in the hip or spine. It is also helpful in
precisely defining the location of the tumor and the extent of osseous involvement.
Histopathology
Pathophysiology
The pathophysiology of osteoid osteoma has been controversial as to whether it is neoplastic or
inflammatory. The presence of atypical cellular and trabecular components support its being a neoplasia.
However, its relatively small size, self-limited nature, and intracellular viral particles (as observed on
electron microscopy) may suggest an inflammatory process.
Pain in osteoid osteoma has been typically attributed to the nidus, with its associated hyperostosis and
neural elements in the reactive fibrous tissue.
Golding described radially oriented trabeculae of surrounding reactive bone, which implied an increased
pressure in the vascular nidus.[48 ] This arrangement of the bony trabeculae was attributed to the stresses
placed on them. This increased pressure due to vasodilatation and edema is thought to directly stimulate
intraosseous nerve endings, generating pain. Schulman et al supported this observation, finding increased
amounts of unmyelinated nerve fibers, with greatest abundance next to arterioles. These fibers were
believed to be sensitive to changes in vascular pressure.[49 ]
Prostaglandins have been implicated and linked to osteoid osteoma. Several authors have even suggested
that they may have a fundamental role in the development of osteoid osteoma. Support is derived from
reports of a 100- to 1000-fold increase in levels of prostaglandins, particularly prostaglandins E2 and I2
(prostacyclin), in the nidus that was reversible on extirpation of the tumor. These prostaglandins and other
mediators of bone formation and inflammation are believed to provide the final common pathway for pain
generation. Furthermore, the dramatic response to salicylates or nonsteroidal anti-inflammatory drugs
(NSAIDs), which affect prostaglandin synthesis, supports the suggested role of prostaglandins in the
pathophysiology of pain.
Healey and Ghelman described 2 pathways of pain generation due to prostaglandins.[50 ]The first involves
permeability and vasodilatory effects, which increase the size and flow of vessels in the bony lesion,
increasing pressure and pain. The second involves its effect in the bradykinin system, which potentiates
pain akin to injured soft tissues.
Pathology
Osteoid osteoma typically consists of a discrete central nidus usually <1 cm with diffuse peripheral
sclerosis. The nidus is usually a distinct, well-circumscribed cavity, surrounded by dense reactive bone of
varying thickness. It is typically cherry red in color and can be shelled out of the surrounding reactive bone.
The nidus varies in consistency from vascular, soft, friable, gritty, and granular to densely sclerotic. During
surgery, an increased number of fine, punctuate vessels and adherent periosteum overlying the lesion may
be observed. Osteoid osteoma is usually cortical and may extend into the periosteal or endosteal surface of
the bone. It is rare in the spongiosa.
On microscopic evaluation, the nidus is typically composed of a mass of irregular osteoid tissues that lie in
a highly vascular stroma of connective tissue containing osteoblastic cells. It consists of irregular lacelike
osteoid and calcified matrix lined by plump osteoblasts and osteoclasts with a well-vascularized but bland
stroma.
The microscopic appearance of osteoid osteoma may vary with the degree of lesional maturity. During the
initial stage of the disease, proliferation occurs in osteoblasts and vascularized spindle cell stroma with
minimal new bone formation. In the intermediate stage, patches of calcified osteoid between the neoplastic
stromal cells appear. The mature stage manifests with densely packed atypical bony trabeculae with
decreased vascularity and stroma.
The histologic stage is not correlated with the patient's clinical picture.
Diagnostic importance
The diagnosis of osteoid osteoma can be confirmed only with pathologic examination.
Percutaneous needle biopsy
Pathologic confirmation of the diagnosis of osteoid osteoma by means of percutaneous needle biopsy yields
reliable results in only 50% of cases.
Use of radionuclide scans in pathologic examination
Use of autoimaging and scintigraphy has increased in the pathologic examination of osteoid osteoma
specimens. Autoimaging helps direct attention to the hottest fragment, which corresponds to the nidus.
Thus, it decreases false-negative reports, which most commonly occur because of sampling error.
Medical Treatment
Initial treatment of osteoid osteoma remains nonoperative, with medications consisting of aspirin or other
NSAIDs. In fact, Barei et al suggested that patients with osteoid osteoma be treated with NSAIDs if they
can tolerate them, because many patients may achieve lasting pain relief with NSAIDs.[9 ]
The response to salicylates is not universal, however; it can vary and is therefore not a reliable sign, as
previously thought. Healey et al noted improved symptoms in 73% of patients, with patients taking only
aspirin, 650-3250 mg/day, to control pain.[50 ]Kirchner et al also reported that the response to salicylates can
vary, from 30% to 75%.[51 ]Pettine et al described substantially decreased pain with aspirin or NSAIDs, with
positive responses in 90% of patients.[11 ]
Response to other NSAIDs, such as naproxen, has also been reported in literature. Saville et al noted good
responses to therapeutic doses of naproxen after trials with aspirin, indomethacin, ibuprofen, and
fenoprofen were tried.[52 ]They noted resolution of pain after 22 months of treatment, with complete
resolution of pain after 33 months. Carpintero-Benitez et al noted a good response of pain to
cyclooxygenase-2 (COX-2) inhibitors, as compared with conventional NSAIDs.[53 ]
Several authors have suggested that because the general mechanism of action of aspirin and NSAIDs is
inhibition of prostaglandin synthesis leading to pain relief, any intervention that decreases the concentration
of prostaglandins in the osteoma will also decrease the related pain.
If medical management is selected, blood counts and serum chemistries should be periodically monitored in
all patients. Sequential radiographs should also be obtained at 3- to 6-month intervals during treatment.
Observed radiographic changes that suggest healing of the lesion are ossification of the nidus and increased
bone formation around the nidus.
Most patients are unable to continue this regimen of treatment. According to Barei et al, the most common
reasons for treatment failure were little tolerance for ongoing pain among young, active patients, who opt
for an aggressive surgical alternative; an initial effect of anti-inflammatory medications that diminishes
over time; and persistent pain.[9 ]
Kneisl et al mentioned several contraindications for NSAID use, including sensitivity to the medications,
progressive deformity of the limb, and uncertainty about the diagnosis. They added the relative
contraindications of patient preference, breakthrough pain with therapeutic doses of medications, and
adverse effects (including GI toxicity, CNS symptoms, and dermatologic manifestations).[54 ]
Traditional Open Surgical Treatment
Timing of Surgery
Timing of surgery has not been an issue for osteoid osteoma anywhere in the body except for the spine.
Mehta and Murray reported that patients with scoliosis reach a critical point after which the continuing
discharge of painful stimuli results in a structural change of the spine that precludes resolution of the
deformity after the tumor is removed.[55 ]In their study, painful symptoms that were present during the
patient's growth spurt were most likely to cause progression of the scoliosis. Furthermore, the patient's age
at the onset of symptoms and the duration of symptoms were the most important determinants at this
critical point.
Pettine et al observed that 15 months was the critical duration of symptoms for antalgic scoliosis to
spontaneously correct after excision.[11 ]In patients with symptoms lasting less than 15 months, scoliosis is
decreased or completely corrected within a short time after excision alone. Age was a less important factor
than symptom duration, but patients who were relatively old at onset of symptoms and those who were
young at time of surgery were most likely to have spontaneous correction of the curve.
Indications for Surgery
Surgical intervention is generally indicated for patients whose pain is unresponsive to medical therapy,
patients who cannot tolerate prolonged use of NSAIDs, and those who are not amenable to activity
restrictions.
Surgery and Surgical Options
Complete surgical excision of the nidus, even if it is intralesional, is the treatment of choice for patients
with osteoid osteoma in whom conservative management fails. It provides immediate relief and is usually
curative. Complete surgical excision is the most predictable way to cure osteoid osteoma and should be the
goal of surgical intervention.
Pettine et al added that the most important determinant for successful surgical removal is the exact
localization of the lesion.[11 ]
Campanacci et al suggested 2 main approaches in open surgical treatment of osteoid osteoma: wide en bloc
resection and unroofing and excision.[56 ]
En bloc resection
En bloc resection of the lesion with surrounding bone is recommended in the treatment of osteoid osteoma,
but this is not always possible. The purpose is to ensure complete removal of the nidus to minimize the risk
of recurrence.
Disadvantages of this procedure include excessive resection of normal bone in the effort to completely
excise the lesion. The procedure is contraindicated in patients with lesions in areas difficult to access, such
as the acetabulum or femoral head and neck, where it leads to substantial morbidity.
Kruger et al suggested that en bloc excision under imaging intensification is the treatment of choice for
epiphyseal lesions.[57 ]
Unroofing and curettage
The procedure of unroofing and curettage entails unroofing of the nidus by gradually removing the
overlying reactive bone, followed by excision with curettes and burrs. It is effective and has a cure rate of
75-100%. Unroofing and curettage is especially helpful in treating lesions in a structurally vital location,
such as the femoral neck, wherein the tumor is eradicated without disrupting the underlying central
sclerotic bone. This approach helps maintain structural support for the area.
Prophylactic internal fixation
Healey et al reported that prophylactic internal fixation is indicated if substantial cortex is resected and if
the remaining bone is weakened.[50 ]
Spinal fusion
Healy et al reported that spinal fusion should be performed only if instability results from excision of the
lesion.[50 ]
Intraoperative Findings and Appearance
Subperiosteal lesions may be visible as a superficial deformation of a few millimeters in size. Changes on
the bone surface in the form of a focal increase in the diameter of the superficial bone vessels, a pink area
of millimetric dimensions, or both may reveal the presence of such lesions.
Intracortical lesions are difficult to localize by just scrutinizing the bone surface if it is covered by thick
periosteum. However, these lesions cause extensive bone reaction that typically surrounds the nidus of the
tumor.
Intra-articular or medullary types cause little or no periosteal reaction; therefore, they are difficult to
identify visually.
Contraindications and Disadvantages
Lesions in anatomically inaccessible areas, such as the femoral head and neck, result in considerable
surgical morbidity, and their removal may cause complications or disability more severe than that
associated with the original condition.
Other disadvantages include difficulties in identifying and localizing the nidus at the time of surgery,
postoperative restriction of activity that may be required after bone is removed, and an awkward anatomic
location of the tumor that may require an extensive surgical approach.
Complications
En bloc surgical resection of the tumor leads to extended hospital stay; perioperative fractures; the need for
bone grafts, internal fixation, or both; periarticular stiffness; and delayed functional recovery.
About 9-28% of osteoid osteomas recur after surgical extirpation, where the rate of local recurrence is
inversely proportional to the aggressiveness of the surgery. Healey et al noted that intralesional resection or
curettage had the highest recurrence rate and that en bloc resection had the lowest rate.[50 ]Several authors
linked this finding to incomplete removal of the nidus. Recurrence is typically observed within 1 year after
excision; hence, the patient should be monitored for a minimum of 1 year.
Proper preoperative and intraoperative localization of the tumor is critical to ensure adequate resection of
the tumor and minimize the likelihood of recurrence. The use of these techniques dramatically reduce the
recurrence rate.
Failure to relieve pain is associated with a bad prognosis, and it most probably indicates incomplete
removal of the tumor. Rosenthal et al noted persistence of symptoms in 30% of cases.[58,59 ]
Surgical Outcome
Direct visualization and intralesional excision of the nidus is associated with a primary cure rate of 100%.
Successful excision substantially eliminates tumor-related pain within hours to days after surgery.
Assenmacher et al described immediate relief of pain in their patients, with a mean symptom-free duration
of 6.6 years after surgery.[60 ]
Minimally Invasive Surgical Treatments
Surgical Options
Radionuclide-guided excision
The use of radionuclides in surgery started in 1949, when attempts were made to facilitate surgery by
taking advantage of the property of certain lesions to concentrate radiopharmaceuticals.
For radionuclide-guided excision, patients undergo bone scintigraphy at diagnosis by using technetium-
99m-labeled hydroxymethylene diphosphonate (HMDP) and dichloromethylene diphosphonate (DMDP).
Three hours before surgery, the radionuclide is given to the patient, followed by control scanning
encompassing the hot spot 1 hour after the injection. A radiation detector probe is then used to locate the
hot spot by using the signal produced.[32,61,62,63,64,65 ]
This method can be used to locate the projection of the nidus with a precision of 2 mm, facilitating excision
of lesions with minimal damage to normal bone. Furthermore, it can reveal the progress of the excision and
the absence of residual pathologic tissue at the end of the operation.[62,63,64,66,67 ]
Disadvantages of this method include the narrowness and depth of the operative field, which causes
difficulty in positioning the probe perpendicular to the bone surface. In addition, narrow probes can cause
false-negative readings and, hence, imprecise localization of the lesion. Also, at the end of the operation,
confirmation of complete removal of the lesion is difficult because of the altered anatomy of the site.
Finally, the surgeon might be unsure if the lesion is completely excised because the probe detects high
radioactivity in perilesional sclerosis.[65 ]
CT-guided percutaneous excision
CT-guided preoperative insertion of a needle is important to localize the nidus of an osteoid osteoma during
surgery. Proper insertion of the needle reduces the amount of bone removed during surgery and reduces the
risk of postoperative fracture.[68 ]Another advantage of this procedure is immediate verification of complete
removal of the nidus with histologic confirmation of the diagnosis.[37 ]
The technique is done with the patient under local anesthesia. It entails identification of the lesion on the
CT scan. Then, with CT guidance, a Kirschner wire is inserted and drilled through the cortex into the nidus.
A small incision is created, a biopsy punch is inserted over the Kirschner wire, and the specimen is
completely removed. Postoperative CT scanning is performed to confirm complete evacuation of the nidus.
Finally, pathologic examination is done to confirm the diagnosis.
CT-guided percutaneous resection has a success rate of 83-100%. Campanacci et al noted a primary cure
rate of 83% after a percutaneous procedure, with an additional 9% cured after a second procedure.
However, they reported a failure rate of 2%, with no change in pain, after percutaneous treatment.[56 ]

Donohue et al observed that preoperative pain resolved within 1-2 weeks after percutaneous treatment, with
no clinical or radiographic evidence of recurrence at a mean follow-up of 17 months (range, 9-43 mo).[69 ]
Complications associated with this procedure include postoperative fracture, limitation of activity and
impaired weight bearing for as long as 3 months after surgery, skin burns due to high rotation speed of the
instrument, muscle hematoma, irritation of adjacent nerves with transient paresis, and osteomyelitis. Sans et
al noted a complication rate of 24% in this procedure.[38 ]
Percutaneous laser photocoagulation
Bown et al first described percutaneous laser photocoagulation in 1983.[70 ]The technique entails CT-guided
localization of the nidus. A bare optical fiber or fibers are inserted directly into the target tissue, followed
by treatment with low levels of power or laser energy (2-4 W) for several minutes. This causes a relatively
predictable area of coagulative necrosis secondary to thermal destruction of the nidus.[71,72 ]
Witt et al quantified the amount of coagulation in relation to the amount of power applied over the lesion.
[73 ]
With 2 W of constant power, the mean axial diameter of coagulation was 3.4 mm with 200 J and was 9.2
mm with 1000 J; the mean longitudinal diameter of coagulation was 4 mm with 200 J and was 11.1 mm
with 1400 J. The maximum effect was reached with the delivery of 1000-1200 J. No alteration in the area
of coagulation was noted with more energy applied. Complete relief of pain was noted within 24-48 hours,
and, at 72 hours, the patients could stop taking analgesics.[73 ]
Lindner et al described a primary cure rate of 93% and a 96% cure rate after the second ablation.[74 ]
Percutaneous radiofrequency coagulation
Percutaneous radiofrequency coagulation is performed by using an electrode placed in the lesion, coupled
with a radiofrequency generator that produces local tissue destruction by converting radiofrequency into
heat.
The technique involves CT-guided insertion of a trocar, followed by application of an electrode. Electrode
placement is then confirmed with CT, and after confirmation, the lesion is heated to 90°C for 4 minutes.
Lesions that are larger than average are treated with 2 passes of radiofrequency.[75 ]
Tillotson et al showed reproducible zones of necrosis of 0.9-1.3 cm in diameter when lesions were heated
to 80°C. Neither varying the duration of heating from 30 seconds to 4 minutes nor increasing the size of the
tip altered the area of necrosis. Furthermore, the extent of the lesion and, therefore, tissue necrosis did not
increase over time (3 wk after the procedure).[76 ]
Lundskog et al showed that osteocyte necrosis occurs at 50°C sustained for 30 seconds. Blood flow limited
heat transmission in bone; therefore, lethal temperature to the tissues could not be sustained over great
distances.[77 ]Microscopic examination showed hemorrhage with a radius of approximately 5 mm extending
from the probe tract. Adjacent bone was intact, and viable cells were seen. Over the next 6 weeks, marrow
fat necrosis and reactive fibrosis replaced this hemorrhage. After 6 weeks, a thin, circular rim of
intramedullary reactive bone surrounded this area of fat necrosis.
Complete or nearly complete relief of pain often occurs within 3 days. Patients are sent home on same day
of surgery, and they have no limitations in weight bearing, though aggressive athletics are restricted for 2-3
months. Patients may then return to normal activities immediately or within 24-48 hours after surgery. Pain
resolves immediately, and limping resolves within 24 hours. Furthermore, this procedure requires only a
small osseous access to allow insertion of the electrode; therefore, no substantial structural weakening of
the bone occurs.
Primary cure rates are 83-94%. Cure with a second ablation procedure is approximately 100%. Rosenthal et
al noted no recurrences in their patients at more than 1 year after the procedure.[58,59 ]
Vanderschueren et al reported factors that decrease or increase risk of treatment failures. Advanced age
(mean, 24 y) and increased number of needle positions during thermocoagulation decrease the risk of
treatment failure. However, young age (mean, 20 y) and a lesion of 10 mm or larger increases the risk of
treatment failure.[78 ]
Percutaneous radiofrequency coagulation is currently the preferred treatment for osteoid osteoma because it
does not require hospitalization, is not associated with complications, and is associated with rapid
convalescence.
The main disadvantages of this procedure are recurrence or persistence of the osteoid osteoma and the lack
of histologic verification. Recurrent lesions can be managed with repeat percutaneous radiofrequency
ablation, but lesions should be confirmed histologically by means of needle biopsy before ablation.[79,80 ]
Lesions that are resistant to percutaneous radiofrequency ablation can easily be treated with open surgery.
Another complication is local skin burns.
Computer-assisted surgery
Computer-assisted surgery is a collection of techniques in which imaging and use of 3-dimensional
tracking devices are combined to improve surgical performance. This surgery is based on initial diagnostic
CT scans that are processed into 3-dimensional images. The volume or surface is then extracted to produce
a computational model of the anatomy.[69,75,81 ]
The technique entails intraoperatively registering the patient to the preoperative image by determining a
rigid-body transformation. Optical trackers mounted on modified surgical instruments are attached to the
patient to allow for intraoperative tracking with an optical system. Given the transformation between
patient and image, the computer displays the 3-dimensional location and orientation of an instrument by
superimposing a graphical representation of the instrument on the preoperative computer-generated image.
The advantage of this technique is that it can provide precise and accurate localization of lesions in bone. It
is useful for small lesions located deep in the cortical bone, where there may be subtle or no surface
changes to guide the surgeon. The procedure is conducted without fluoroscopy; fluoroscopy is used only at
completion of the operation to document bone-tunnel placement. The percutaneous technique can be used
in unison with this procedure.
Complications
Incomplete resection is a real complication of minimally invasive procedures. Roger et al observed
incomplete resection in 35.7% of patients, as assessed by immediate follow-up scintigraphy following CT-
guided percutaneous excision. These patients needed an immediate second resection to extirpate the lesion
and relieve pain.[82 ]
Recurrence is frequently linked to incomplete resection of the tumor. Rosenthal et al[58,59 ]and Barei et al[9 ]
noted a 12% recurrence rate in patients who underwent percutaneous radiofrequency ablation. This rate was
not significantly different from that associated with surgical excision of the nidus. Atar et al stated that this
was also the case with CT-guided percutaneous excision.[23 ]
Rosenthal et al noted that in 23% of patients, symptoms persisted following percutaneous radiofrequency
ablation. This was significantly lower than the 30% rate associated with operative excision.[58,59 ]
Summary
Details of osteoid osteoma may be summarized as follows:
• Bergstrand first described osteoid osteoma in 1930, and Jaffe first recognized it as a separate
entity in 1935
• Osteoid osteoma is a benign osteoblastic process (<1.5-2 cm) characterized by an osteoid-rich
nidus in highly loose, vascular connective tissue.
• Osteoid osteoma accounts for approximately 10% of symptomatic benign bone tumors and 5% of
all primary bone tumors.
• This lesion is a condition of youth, as 90% of cases occur in patients younger than 25 years.
• A particular male preponderance is observed, with a male-to-female ratio of 2-3:1.
• The tumor occurs in the cortex of shafts of long bones in 80-90% of cases. It most commonly
affects the lower extremity. The spine is involved in 7-20% of cases.
• The natural history is resolution of pain and healing of the lesion. The course is unpredictable, and
intervals for pain resolution are sometimes 6-15 years.
• Two stages are described: (1) an acute, painful stage lasting 18-36 months, during which patients
require steady use of analgesics, and (2) a recovery stage involving healing of the nidus, which
usually lasts 3-7 years.
• Pain is the principal symptom. It is the worst at night and diminishes in the morning in 95% of
patients. The pain dramatically responds to salicylates or NSAIDs in 50-75% of patients. Patients
may also present with painful scoliosis, swelling, monoarticular arthritis, macrodactyly, clubbing,
and painless swelling.
• Tenderness is present in 62% of patients. Local warmth and erythema are possible. Other signs
include joint effusion, soft-tissue swelling, contractures, and soft-tissue masses. Neurologic
abnormalities are possible in patients with lesions involving the spine.
• The diagnostic delay is typically 11.8-36 months.
• Blood and chemistry results are normal. Increased levels of prostaglandin metabolites, such as
prostaglandin E1, I2, and F1 alpha, can be 100-1000 times normal.
• The typical radiographic appearance is a radiolucent area of about 1 cm in diameter, with a center
that is sometimes calcified. Variation in radiologic appearances is possible.
• Bone scanning shows a nonspecific but intense, well-defined uptake of activity that represents a
hot spot.
• CT scanning shows a circumscribed annular lesion with a double-attenuation sign. CT findings
help to confirm the diagnosis in 74% of patients, with an accuracy rate of 90% for extra-articular
lesions.
• MRI shows homogeneous enhancement with a ring-enhancement sign. Its intensity is proportional
to the extent of the remaining part of the vascularized nidus. The potential rate of missed diagnosis
is 30%.
• Preoperative localization is the most important determinant of successful surgical removal.
• Intraoperative localization aids the surgeon in localizing and identifying the lesion to minimize
bone resection and to ensure complete excision.
• The gross appearance of the lesions is that of a distinct, well-circumscribed cavity surrounded by
dense reactive bone. It is cherry red and can be shelled out of the surrounding reactive bone.
• The microscopic appearance is irregular, lacelike osteoid and calcified matrix lined by plump
osteoblasts and osteoclasts with a well-vascularized but bland stroma.
• Initial treatment is medical and consists of aspirin and NSAIDs. This produces a 30-90% response
rate.
 • Traditional open surgical treatment consists of en bloc resection and unroofing and curettage,
which is the treatment of choice. The rate of primary cure is approximately 100%. Disadvantages
include perioperative morbidity, extended hospital stay, perioperative fractures, a need for bone
grafts or internal fixation, periarticular stiffness, and delayed functional recovery. The recurrence
rate is 9-28%.
• Minimally invasive surgical treatments include radionuclide-guided excision, CT-guided
percutaneous excision, percutaneous laser photocoagulation, percutaneous radiofrequency
coagulation, and computer-assisted surgery. Success rates can reach approximately 100%.
Disadvantages include incomplete resection in 35% of patients, persistence of symptoms in 23%,
and recurrence in 12%.
Multimedia

Media file 1: Anteroposterior (AP) and lateral radiographs of osteoid osteoma. Courtesy of Cincinnati
Children's Hospital Medical Center, Department of Pediatric Orthopaedics.

Media file 2: Axial CT scan shows osteoid osteoma. Courtesy of Cincinnati Children's Hospital Medical
Center, Department of Pediatric Orthopaedics.
Media file 3: Reconstructed axial CT scan shows osteoid osteoma. Courtesy of Cincinnati Children's
Hospital Medical Center, Department of Pediatric Orthopaedics.

Media file 4: Coronal CT scan shows osteoid osteoma. Courtesy of Cincinnati Children's Hospital Medical
Center, Department of Pediatric Orthopaedics.

Media file 5: Sagittal CT scan shows osteoid osteoma. Courtesy of Cincinnati Children's Hospital Medical
Center, Department of Pediatric Orthopaedics.
Media file 6: MRI shows osteoid osteoma. Courtesy of Cincinnati Children's Hospital Medical Center,
Department of Pediatric Orthopaedics.

Media file 7: MRI shows osteoid osteoma. Courtesy of Cincinnati Children's Hospital Medical Center,
Department of Pediatric Orthopaedics.
References
1. Bergstrand H. Uber eine eigenartige, warscheinlich bisher nicht beschriebene osteoblastische
Krankheit in den langen Knochen in der Hand und des Fusses. Acta Radiol 1930; 11: 596-613.
2. Jaffe HL. Osteoid osteoma. A benign osteoblastic tumor composed of osteoid and atypical
bone. Arch Surg. 1935;31:709-728.
3. Gonzalez G, Abril JC, Mediero IG, Epeldegui T. Osteoid osteoma with a multicentric nidus. Int
Orthop. 1996;20(1):61-3. [Medline].
4. Greenspan A. Benign bone-forming lesions: osteoma, osteoid osteoma, and osteoblastoma.
Clinical, imaging, pathologic, and differential considerations. Skeletal
Radiol. Oct 1993;22(7):485-500. [Medline].
5. Iceton J, Rang M. An osteoid osteoma in an open distal femoral epiphysis. A case report. Clin
Orthop Relat Res. May 1986;162-5. [Medline].
6. Marcove RC, Heelan RT, Huvos AG, et al. Osteoid osteoma. Diagnosis, localization, and
treatment. Clin Orthop Relat Res. Jun 1991;197-201. [Medline].
7. Lenke LG, Sutherland CJ, Gilula LA. Osteoid osteoma of the proximal femur: CT-guided
preoperative localization. Orthopedics. Mar 1994;17(3):289-92. [Medline].
8. Ebrahimzadeh MH, Ahmadzadeh-Chabock H, Ebrahimzadeh AR. Osteoid osteoma: a diagnosis
for radicular pain of extremities. Orthopedics. Nov 2009;32(11):821. [Medline].
9. Barei DP, Moreau G, Scarborough MT, Neel MD. Percutaneous radiofrequency thermal ablation
of osteoid osteoma. Operative Tech Orthop. Apr 1999;9(2):72-8. [Medline].
10. Sproule JA, Khan F, Fogarty EE. Osteoid osteoma: painful enlargement of the second toe. Arch
Orthop Trauma Surg. Jun 2004;124 (5):354-6. [Medline].
11. Pettine KA, Klassen RA. Osteoid-osteoma and osteoblastoma of the spine. J Bone Joint Surg
Am. Mar 1986;68(3):354-61. [Medline].
12. Zileli M, Cagli S, Basdemir G, Ersahin Y. Osteoid osteoma and osteoblastoma of the
spine. Neurosurg Focus. Nov 2003;15 (5):E5. [Medline].
13. LinksKan P, Schmidt MH. Osteoid osteoma and osteoblastoma of the spine (review). Neurosurg
Clin N Am. Jan, 2008;19(1):65-70. [Medline].
14. Burn SC, Ansorge O, Zeller R, Drake JM. Management of osteoblastoma and osteoid osteoma of
the spine in childhood. J Neurosurg Pediatr. Nov 2009;4(5):434-8. [Medline].
15. Wells RG, Miller JH, Sty JR. Scintigraphic patterns in osteoid osteoma and spondylolysis. Clin
Nucl Med. Jan 1987;12(1):39-44. [Medline].
16. Bilgin SS, Yildiz Y, Guclu B, Saglik Y. Osteoid osteoma in the hand: an evaluation of eight
patients. Acta Orthop Traumatol Turc. 2004;38 (3):206-11. [Medline].
17. Kalb K, Schlor U, Meier M, et al. Osteoid osteoma of the hand and wrist [in German]. Handchir
Mikrochir Plast Chir. Dec 2004;36(6):405-10. [Medline].
18. Nanni M, Pantalone O, Zappala A, et al. Diagnostic approach to a rare case of osteoid osteoma of
the astragalus. Rays. Apr-Jun 2004;29 (2):217-21. [Medline].
19. Frassica FJ, Waltrip RL, Sponseller PD, et al. Clinicopathologic features and treatment of osteoid
osteoma and osteoblastoma in children and adolescents. Orthop Clin North
Am. Jul 1996;27(3):559-74. [Medline].
20. Donkol RH, Al-Nammi A, Moghazi K. Efficacy of percutaneous radiofrequency ablation of
osteoid osteoma in children. Pediatr Radiol. Feb 2008;38(2):180-5. [Medline].
21. Szypryt EP, Hardy JG, Colton CL. An improved technique of intra-operative bone scanning. J
Bone Joint Surg Br. Aug 1986;68(4):643-6. [Medline].
22. de Chadarévian JP, Katsetos CD, Pascasio JM, et al. Histological study of osteoid osteoma's blood
supply. Pediatr Dev Pathol. Sep-Oct 2007;10(5):358-68. [Medline].
23. Atar D, Lehman WB, Grant AD. Tips of the trade. Computerized tomography--guided excision of
osteoid osteoma. Orthop Rev. Dec 1992;21(12):1457-8. [Medline].
24. Garcia-Vivar ML, Galindez E, Arostegui J, et al. Chronic monoarthritis caused by osteoid osteoma
[in Spanish]. An Med Interna. Jul 1996;13(7):344-6. [Medline].
25. Burger IM, McCarthy EF. Phalangeal osteoid osteomas in the hand: a diagnostic problem. Clin
Orthop. Oct 2004;427:198-203. [Medline].
26. Janin Y, Epstein JA, Carras R, Khan A. Osteoid osteomas and osteoblastomas of the
spine. Neurosurgery. Jan 1981;8(1):31-8. [Medline].
27. MacLellan DI, Wilson FC Jr. Osteoid osteoma of the spine. A review of the literature and report
of six new cases. J Bone Joint Surg Am. Jan 1967;49(1):111-21. [Medline].
28. Georgoulis AD, Papageorgiou CD, Moebius UG, et al. The diagnostic dilemma created by osteoid
osteoma that presents as knee pain. Arthroscopy. Jan 2002;18(1):32-7. [Medline].
29. Meire E, Hoogmartens M, De Roo M, et al. The peroperative use of the mobile gamma camera for
the localization of spinal osteoid osteoma. Acta Orthop Belg. May-Jun 1983;49(3):384-
90. [Medline].
30. Rinsky LA, Goris M, Bleck EE, et al. Intraoperative skeletal scintigraphy for localization of
osteoid-osteoma in the spine. Case report. J Bone Joint Surg Am. Jan 1980;62(1):143-
4. [Medline].
31. Swee RG, McLeod RA, Beabout JW. Osteoid osteoma. Detection, diagnosis, and
localization. Radiology. Jan 1979;130(1):117-23. [Medline].
32. Israeli A, Zwas ST, Horoszowski H, Farine I. Use of radionuclide method in preoperative and
intraoperative diagnosis of osteoid osteoma of the spine. Case report. Clin Orthop Relat
Res. May 1983;194-6. [Medline].
33. Osebold WR, Lester EL, Hurley JH, Vincent RL. Intraoperative use of the mobile gamma camera
in localizing and excising osteoid osteomas of the spine. Spine. Oct 1 1993;18(13):1816-
28. [Medline].
34. Renzoni SA, Convery FR, Ashburn W, Vasquez TE. Intraoperative osteoscintigraphy as an aid to
bone biopsy. Clin Nucl Med. Sep 1986;11(9):619-20. [Medline].
35. Wioland M, Gaillard JF, Sergent A. Intraoperative bone scintigraphy in orthopaedic
surgery. Biomed Pharmacother. 1991;45(10):429-34. [Medline].
36. Haddad E, Ghanem I, Wicart P, et al. Percutaneous computed tomography-guided thermal
ablation of osteoid osteoma. Rev Chir Orthop Reparatrice Appar Mot. Nov 2004;90 (7):599-
606. [Medline].
37. Peyser A, Porat S, Sasson T, et al. CT-guided excision of osteoid
osteoma. Harefuah. Apr 1999;136 (7):540-2. [Medline].
38. Sans N, Galy-Fourcade D, Assoun J, et al. Osteoid osteoma: CT-guided percutaneous resection
and follow-up in 38 patients. Radiology. Sep 1999;212(3):687-92. [Medline].
39. Szendroi M, Killo K, Antal I, et al. Intraarticular osteoid osteoma: clinical features, imaging
results, and comparison with extraarticular localization. J Rheumatol. May 2004;31 (5):957-
64. [Medline].
40. Athwal GS, Pichora DR, Ellis RE, Rudan JF. A computer-assisted guidance technique for the
localization and excision of osteoid osteoma. Orthopedics. Feb 2004;27(2):195-7. [Medline].
41. Gaeta M, Minutoli E, Pandolfo I, et al. Magnetic resonance imaging findings of osteoid osteoma
of the proximal femur. Eur Radiol. Sep 2004;14 (9):1582-9. [Medline].
42. Hachem K, Haddad S, Aoun N, et al. MRI in the diagnosis of osteoid osteoma [in French]. J
Radiol. Sep 1997;78(9):635-41. [Medline].
43. Youssef BA, Haddad MC, Zahrani A, et al. Osteoid osteoma and osteoblastoma: MRI appearances
and the significance of ring enhancement. Eur Radiol. 1996;6(3):291-6. [Medline].
44. Assoun J, Richardi G, Railhac JJ, Baunin C, Fajadet P, Giron J. Osteoid osteoma: MR imaging
versus CT. Radiology. Apr 1994;191(1):217-23. [Medline].
45. Guzey FK, Seyithanoglu MH, Sencer A, et al. Vertebral osteoid osteoma associated with
paravertebral soft-tissue changes on magnetic resonance imaging. Report of two cases. J
Neurosurg Spine. May 2004;100 (5):532-6. [Medline].
46. Davies M, Cassar-Pullicino VN, Davies AM, et al. The diagnostic accuracy of MR imaging in
osteoid osteoma. Skeletal Radiol. Oct 2002;31(10):559-69. [Medline].
47. Klonecke AS, Licho R, McDougall IR. A technique for intraoperative bone scintigraphy. A report
of 17 cases. Clin Nucl Med. Jul 1991;16(7):482-6. [Medline].
48. GOLDING JS. The natural history of osteoid osteoma; with a report of twenty cases. J Bone Joint
Surg Br. May 1954;36-B(2):218-29. [Medline].
49. Schulman L, Dorfman HD. Nerve fibers in osteoid osteoma. J Bone Joint Surg
Am. Oct 1970;52(7):1351-6. [Medline].
50. Healey JH, Ghelman B. Osteoid osteoma and osteoblastoma. Current concepts and recent
advances. Clin Orthop Relat Res. Mar 1986;76-85. [Medline].
51. Kirchner B, Hillmann A, Lottes G, et al. Intraoperative, probe-guided curettage of osteoid
osteoma. Eur J Nucl Med. Jul 1993;20(7):609-13. [Medline].
52. Saville PD. A medical option for the treatment of osteoid osteoma. Arthritis
Rheum. Dec 1980;23(12):1409-11. [Medline].
53. Carpintero-Benitez P, Aguirre MA, Serrano MA, Lluch M. Effect of rofecoxib on pain caused by
osteoid osteoma. Orthopaedics. Nov 2004;27 (11):1188-91. [Medline].
54. Kneisl JS, Simon MA. Medical management compared with operative treatment for osteoid-
osteoma. J Bone Joint Surg Am. Feb 1992;74(2):179-85. [Medline].
55. Mehta MH. Pain provoked scoliosis. Observations on the evolution of the deformity. Clin Orthop
Relat Res. Sep 1978;(135):58-65. [Medline].
56. Campanacci M, Ruggieri P, Gasbarrini A, et al. Osteoid osteoma. Direct visual identification and
intralesional excision of the nidus with minimal removal of bone. J Bone Joint Surg
Br. Sep 1999;81(5):814-20. [Medline].
57. Kruger GD, Rock MG. Osteoid osteoma of the distal femoral epiphysis. A case report. Clin
Orthop Relat Res. Sep 1987;203-9. [Medline].
58. Rosenthal DI, Hornicek FJ, Wolfe MW, et al. Percutaneous radiofrequency coagulation of osteoid
osteoma compared with operative treatment. J Bone Joint Surg Am. Jun 1998;80(6):815-
21. [Medline].
59. Rosenthal DI, Springfield DS, Gebhardt MC, et al. Osteoid osteoma: percutaneous radio-
frequency ablation. Radiology. Nov 1995;197(2):451-4. [Medline].
60. Assenmacher S, Voggenreiter G, Klaes W, Nast-Kolb D. Osteoid osteoma--a diagnostic and
therapeutic problem? [in German]. Chirurg. Mar 2000;71(3):319-25. [Medline].
61. Gore DR, Mueller HA. Osteoid-osteoma of the spine with localization aided by 99 mTc-
polyphosphate bone scan. Case report. Clin Orthop Relat Res. Nov-Dec 1975;132-4. [Medline].
62. Todd BD, Godfrey LW, Bodley RN. Intraoperative radioactive localization of an osteoid osteoma:
a useful variation in technique. Br J Radiol. Feb 1989;62(734):187-9. [Medline].
63. Vigorita VJ, Ghelman B. Localization of osteoid osteomas--use of radionuclide scanning and
autoimaging in identifying the nidus. Am J Clin Pathol. Feb 1983;79(2):223-5. [Medline].
64. Wioland M, Sergent-Alaoui A. Didactic review of 175 radionuclide-guided excisions of osteoid
osteomas. Eur J Nucl Med. Aug 1996;23(8):1003-11. [Medline].
65. Nachin P, Gille P, Aubert D, et al. Advantages and disadvantages of peroperative isotopic
localization in the excision of osteoid osteoma. Considerations apropos of 6 cases [in
French]. Chir Pediatr. 1986;27(2):65-8. [Medline].
66. De Boeck H, Casteleyn PP, Bossuyt A, Jacobs A. Intraoperative radioactive localization of small
bone tumours. Int Orthop. 1992;16(2):172-5. [Medline].
67. Gille P, Nachin P, Aubert D, et al. Intraoperative radioactive localization of osteoid osteomas: four
case reports. J Pediatr Orthop. Sep-Oct 1986;6(5):596-9. [Medline].
68. Gangi A, Dietemann JL, Guth S, et al. Percutaneous laser photocoagulation of spinal osteoid
osteomas under CT guidance. AJNR Am J Neuroradiol. Nov-Dec 1998;19(10):1955-8. [Medline].
69. Donahue F, Ahmad A, Mnaymneh W, Pevsner NH. Osteoid osteoma. Computed tomography
guided percutaneous excision. Clin Orthop Relat Res. Sep 1999;191-6. [Medline].
70. Bown SG. Phototherapy in tumors. World J Surg. Nov 1983;7(6):700-9. [Medline].
71. Gangi A, Gasser B, De Unamuno S, Fogarrassy E, Fuchs C, Siffert P. New Trends in Interstitial
Laser Photocoagulation of Bones. Semin Musculoskelet Radiol. 1997;1(2):331-338. [Medline].
72. Motamedi D, Learch TJ, Ishimitsu DN, Motamedi K, Katz MD, Brien EW, et al. Thermal ablation
of osteoid osteoma: overview and step-by-step guide. Radiographics. Nov 2009;29(7):2127-
41. [Medline].
73. Witt JD, Hall-Craggs MA, Ripley P, et al. Interstitial laser photocoagulation for the treatment of
osteoid osteoma. J Bone Joint Surg Br. Nov 2000;82(8):1125-8. [Medline].
74. Lindner NJ, Ozaki T, Roedl R, et al. Percutaneous radiofrequency ablation in osteoid osteoma. J
Bone Joint Surg Br. Apr 2001;83(3):391-6. [Medline].
75. Cioni R, Armillotta N, Bargellini I, et al. CT-guided radiofrequency ablation of osteoid osteoma:
long-term results. Eur Radiol. Jul 2004;14 (7):1203-8. [Medline].
76. Tillotson CL, Rosenberg AE, Rosenthal DI. Controlled thermal injury of bone. Report of a
percutaneous technique using radiofrequency electrode and generator. Invest
Radiol. Nov 1989;24(11):888-92. [Medline].
77. Lundskog J. Heat and bone tissue. An experimental investigation of the thermal properties of bone
and threshold levels for thermal injury. Scand J Plast Reconstr Surg. 1972;9:1-80. [Medline].
 78. Vanderschueren GM, Taminiau AH, Obermann WR, et al. Osteoid osteoma: factors for increased
risk of unsuccessful thermal coagulation. Radiology. Dec 2004;233 (3):757-62. [Medline].
79. Akhlaghpoor S, Aziz Ahari A, Ahmadi SA, Arjmand Shabestari A, Gohari Moghaddam K,
Alinaghizadeh MR. Histological evaluation of drill fragments obtained during osteoid osteoma
radiofrequency ablation. Skeletal Radiol. May 2010;39(5):451-5. [Medline].
80. Volkmer D, Sichlau M, Rapp TB. The use of radiofrequency ablation in the treatment of
musculoskeletal tumors. J Am Acad Orthop Surg. Dec 2009;17(12):737-43. [Medline].
81. Powell MF, DiNobile D, Reddy AS. C-arm fluoroscopic cone beam CT for guidance of minimally
invasive spine interventions. Pain Physician. Jan 2010;13(1):51-9. [Medline].
82. Roger B, Bellin MF, Wioland M, Grenier P. Osteoid osteoma: CT-guided percutaneous excision
confirmed with immediate follow-up scintigraphy in 16
outpatients. Radiology. Oct 1996;201(1):239-42. [Medline].
Keywords
osteoid osteoma, osteoma, osteoid osteomas, bone tumor, osteoblast, spinal tumor, spinal tumors, femur
tumor, tibia tumor, humerus tumor, benign tumor, hip tumor, scoliosis
Contributor Information and Disclosures
Author
Gerard Librodo, MD, Consulting Staff, Flinthills Orthopaedics
Gerard Librodo, MD is a member of the following medical societies: American Medical Association and
North American Spine Society
Disclosure: Nothing to disclose.
Coauthor(s)
Charles T Mehlman, DO, MPH, Professor of Pediatrics and Pediatric Orthopedic Surgery, Division of
Pediatric Orthopedic Surgery, Director, Musculoskeletal Outcomes Research, Cincinnati Children's
Hospital Medical Center
Charles T Mehlman, DO, MPH is a member of the following medical societies: American Academy of
Pediatrics, American Fracture Association, American Medical Association, American Orthopaedic Foot
and Ankle Society, American Osteopathic Association, Arthroscopy Association of North America, North
American Spine Society, Ohio State Medical Association, Pediatric Orthopaedic Society of North America,
and Scoliosis Research Society
Disclosure: Nothing to disclose.
Medical Editor
Miguel A Schmitz, MD, Consulting Surgeon, Department of Orthopedics, Klamath Orthopedic and Sports
Medicine Clinic
Miguel A Schmitz, MD is a member of the following medical societies: American Academy of
Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, Arthroscopy Association of
North America, and North American Spine Society
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Managing Editor
Ian D Dickey, MD, FRCSC, Adjunct Professor, Department of Chemical and Biological Engineering,
University of Maine; Consulting Staff, Adult Reconstruction, Orthopedic Oncology, Department of
Orthopedics, Eastern Maine Medical Center
Ian D Dickey, MD, FRCSC is a member of the following medical societies: American Academy of
Orthopaedic Surgeons, British Columbia Medical Association, Canadian Medical Association, and Royal
College of Physicians and Surgeons of Canada
Disclosure: Stryker Orthopaedics Consulting fee Consulting; Sanofi-Aventis Honoraria Speaking and
teaching
CME Editor
Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School;
Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital
Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of
Orthopaedic Surgeons
Disclosure: Nothing to disclose.
Chief Editor
Harris Gellman, MD, Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of
Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of
Miami School of Medicine
Harris Gellman, MD is a member of the following medical societies: American Academy of Medical
Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American
Society for Surgery of the Hand, and Arkansas Medical Society
Disclosure: Nothing to disclose.
Further Reading
Related eMedicine topics:

Osteoid Osteoma [Pathology]

Osteoid Osteoma [Radiology]

Osteoblastoma [Orthopedic Surgery]

Osteoblastoma [Radiology]

Spinal Tumors [Orthopedic Surgery]

Skull Base Tumors [Neurosurgery]

© 1994-2010 by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)