Orthopedics

CME Review Article 

Osteoid Osteoma

Petros J. Boscainos, MD, FRCSEd; Gerard R. Cousins, MBChB, BSc(MedSci), MRCS; Rajiv Kulshreshtha, MBBS, MRCS; T. Barry Oliver, MBChB, MRCP, FRCR; Panayiotis J. Papagelopoulos, MD, DSC

Abstract

Educational Objectives

As a result of reading this article, physicians should be able to:

Discuss the clinical presentation of and different imaging modality options for suspected osteoid osteomas.

2. Develop an insight into the histopathology and histochemistry of osteoid osteomas.

3. Use diagnostic processes in the differential diagnosis of suspected osteoid osteomas.

4. Apply current treatment depending on the location and accessibility of the lesion.

 

Osteoid osteoma is the third most common benign bone tumor. The authors describe the clinical presentation, diagnostic investigations, differential diagnosis, histopathology, and treatment options for this condition, including a comprehensive review of the literature. Osteoid osteomas have wide variations in presentation and tend to present in the second decade of life, with pain that is worse at night and is relieved by salicylates. Plain radiographs and computed tomography scans are the mainstay of imaging; however, bone scintigraphy, single-photon emission computed tomography, magnetic resonance imaging, and sonography are also used. Osteoid osteomas consist of a nidus with surrounding sclerotic bone. The differential diagnosis covers a wide range of conditions due to the variable presentation of osteoid osteoma. The natural history is for regression to occur within 6 to 15 years with no treatment; however, this can be reduced to 2 to 3 years with the use of aspirin and non-steroidal anti-inflammatory drugs. Computed tomography–guided percutaneous techniques, including trephine excision, cryoablation, radiofrequency ablation, and laser thermocoagulation, are described.

 

The authors are from the Department of Trauma and Orthopaedic Surgery (PJB, GRC, RK), Perth Royal Infirmary, NHS Tayside, Perth, Scotland; Department of Radiology (TBO), Ninewells Hospital, NHS Tayside, Dundee, United Kingdom; and the Department of Orthopaedics (PJP), Athens University Medical School, Athens, Greece.

The material presented in any Keck School of Medicine of USC continuing education activity does not necessarily reflect the views and opinions of Orthopedics or Keck School of Medicine of USC. Neither Orthopedics nor Keck School of Medicine of USC nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.

The authors would like to thank Dr Elaine MacDuff, Western Infirmary, Glasgow, United Kingdom, for providing the image of the hematoxylin-eosin stain.

Correspondence should be addressed to: Petros J. Boscainos, MD, FRCSEd, Department of Trauma and Orthopaedic Surgery, Perth Royal Infirmary, NHS Tayside, Taymount Terrace, Perth, United Kingdom, PH1 1NX (petros.boscainos@nhs.net).

 

 CME ACCREDITATION
This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Keck School of Medicine of USC and Orthopedics. Keck School of Medicine of USC is accredited by the ACCME to provide continuing medical education for physicians.

Keck School of Medicine of USC designates this Journal-based CME activity for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

This CME activity is primarily targeted to orthopedic surgeons, hand surgeons, head and neck surgeons, trauma surgeons, physical medicine specialists, and rheumatologists. There is no specific background requirement for participants taking this activity.

FULL DISCLOSURE POLICY
In accordance with the Accreditation Council for Continuing Medical Education’s Standards for Commercial Support, all CME providers are required to disclose to the activity audience the relevant financial relationships of the planners, teachers, and authors involved in the development of CME content. An individual has a relevant financial relationship if he or she has a financial relationship in any amount occurring in the last 12 months with a commercial interest whose products or services are discussed in the CME activity content over which the individual has control.
The authors have no relevant financial relationships to disclose. Dr Aboulafia, CME Editor, has no relevant financial relationships to disclose. Dr D’Ambrosia, Editor-in-Chief, has no relevant financial relationships to disclose. The staff of Orthopedics have no relevant financial relationships to disclose.

UNLABELED AND INVESTIGATIONAL USAGE
The audience is advised that this continuing medical education activity may contain references to unlabeled uses of FDA-approved products or to products not approved by the FDA for use in the United States. The faculty members have been made aware of their obligation to disclose such usage. 

 


Abstract

Educational Objectives

As a result of reading this article, physicians should be able to:

Discuss the clinical presentation of and different imaging modality options for suspected osteoid osteomas.

2. Develop an insight into the histopathology and histochemistry of osteoid osteomas.

3. Use diagnostic processes in the differential diagnosis of suspected osteoid osteomas.

4. Apply current treatment depending on the location and accessibility of the lesion.

 

Osteoid osteoma is the third most common benign bone tumor. The authors describe the clinical presentation, diagnostic investigations, differential diagnosis, histopathology, and treatment options for this condition, including a comprehensive review of the literature. Osteoid osteomas have wide variations in presentation and tend to present in the second decade of life, with pain that is worse at night and is relieved by salicylates. Plain radiographs and computed tomography scans are the mainstay of imaging; however, bone scintigraphy, single-photon emission computed tomography, magnetic resonance imaging, and sonography are also used. Osteoid osteomas consist of a nidus with surrounding sclerotic bone. The differential diagnosis covers a wide range of conditions due to the variable presentation of osteoid osteoma. The natural history is for regression to occur within 6 to 15 years with no treatment; however, this can be reduced to 2 to 3 years with the use of aspirin and non-steroidal anti-inflammatory drugs. Computed tomography–guided percutaneous techniques, including trephine excision, cryoablation, radiofrequency ablation, and laser thermocoagulation, are described.

 

The authors are from the Department of Trauma and Orthopaedic Surgery (PJB, GRC, RK), Perth Royal Infirmary, NHS Tayside, Perth, Scotland; Department of Radiology (TBO), Ninewells Hospital, NHS Tayside, Dundee, United Kingdom; and the Department of Orthopaedics (PJP), Athens University Medical School, Athens, Greece.

The material presented in any Keck School of Medicine of USC continuing education activity does not necessarily reflect the views and opinions of Orthopedics or Keck School of Medicine of USC. Neither Orthopedics nor Keck School of Medicine of USC nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.

The authors would like to thank Dr Elaine MacDuff, Western Infirmary, Glasgow, United Kingdom, for providing the image of the hematoxylin-eosin stain.

Correspondence should be addressed to: Petros J. Boscainos, MD, FRCSEd, Department of Trauma and Orthopaedic Surgery, Perth Royal Infirmary, NHS Tayside, Taymount Terrace, Perth, United Kingdom, PH1 1NX (petros.boscainos@nhs.net).

 

 CME ACCREDITATION
This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Keck School of Medicine of USC and Orthopedics. Keck School of Medicine of USC is accredited by the ACCME to provide continuing medical education for physicians.

Keck School of Medicine of USC designates this Journal-based CME activity for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

This CME activity is primarily targeted to orthopedic surgeons, hand surgeons, head and neck surgeons, trauma surgeons, physical medicine specialists, and rheumatologists. There is no specific background requirement for participants taking this activity.

FULL DISCLOSURE POLICY
In accordance with the Accreditation Council for Continuing Medical Education’s Standards for Commercial Support, all CME providers are required to disclose to the activity audience the relevant financial relationships of the planners, teachers, and authors involved in the development of CME content. An individual has a relevant financial relationship if he or she has a financial relationship in any amount occurring in the last 12 months with a commercial interest whose products or services are discussed in the CME activity content over which the individual has control.
The authors have no relevant financial relationships to disclose. Dr Aboulafia, CME Editor, has no relevant financial relationships to disclose. Dr D’Ambrosia, Editor-in-Chief, has no relevant financial relationships to disclose. The staff of Orthopedics have no relevant financial relationships to disclose.

UNLABELED AND INVESTIGATIONAL USAGE
The audience is advised that this continuing medical education activity may contain references to unlabeled uses of FDA-approved products or to products not approved by the FDA for use in the United States. The faculty members have been made aware of their obligation to disclose such usage. 

 


Osteoid osteoma is a small, distinctive, nonprogressive, benign osteoblastic lesion that is usually accompanied by severe pain. Jaffe1 was the first to report the identification of this osteoblastic lesion in 1935. As the third most common biopsy-analyzed benign bone tumor after osteochondroma and nonossifying fibroma, osteoid osteoma is a relatively common lesion. It represents 11% to 14% of benign bone tumors. Two percent to 3% of excised primary bone tumors are osteoid osteomas.2,3

Clinical Presentation

Osteoid osteoma can manifest at any age, but the majority of patients are aged between 5 and 20 years, with 50% of patients aged between 10 and 20 years.4,5 Osteoid osteomas are 1.6 to 4 times more prevalent in males.4 In the majority of cases, osteoid osteoma occurs in long bones, affecting the metaphysis or diaphysis. The most common loci are the femur and the tibia, with the most characteristic site being the femoral neck and the intertrochanteric region.4 Rarely, it also involves the epiphyseal and intracapsular aspect of long bones (known as intraarticular osteoid osteomas). Less commonly affected are the spine and the small bones of the hand and feet. It can involve the talus, predominantly the talar neck. Flat bones in the body and the skull are rarely affected. Osteoid osteoma is usually localized within the bone cortex. Subcortical, intracortical, and intraperiosteal osteoid osteomas have been described. Osteoid osteomas of the spine account for approximately 6% of cases and almost always involve the posterior arch area close to the pedicles.6,7 The lumbar spine is the most commonly affected region. Multiple osteoid osteoma nidi in the same or different bones are rare.8,9

Pain is the most common clinical presentation. Its usual characteristics are dull, unremitting, initially mild and intermittent pain that increases in intensity and persistence over time. It tends to become increasingly severe at night and is usually relieved by salicylates and nonsteroidal anti-inflammatory drugs (NSAIDs). The indolent nature of early osteoid osteoma may result in delayed presentation. Swelling, erythema, and tenderness may be present in bones in subcutaneous locations.5 Referred pain and muscular atrophy may result in the misdiagnosis of a neurological disorder.10 This observation is common in patients who have a painful osteoid osteoma in posterior elements of the spine, where a postural scoliosis is found due to paravertebral muscle spasm but is reversible after treatment.4

Osteoid osteomas in the region of the proximal femur or pelvis may present with symptoms of knee pain, and the diagnosis may require a bone scan. Intra- or juxta-articular lesions are commonly associated with synovitis.11 Joint pain with flexion contracture, abated range of motion, and antalgic gait can be a clinical pattern of an intra-articular osteoid osteoma.5 In children, the most common presenting symptom is nocturnal pain. In a young child with an osteoid osteoma, a limp may be the only symptom. If the lesion is close to an open physis, it can cause lengthening, angular deformity, or both of the extremity.4

Imaging

Plain Radiographs

Plain radiographs are the initial imaging study of choice. The osteoid osteoma appears as a small, radiolucent nidus (usually less than 1 cm) surrounded by a variable area of sclerotic bone or cortical thickening (Figure 1). The nidus can be difficult to detect when it is obscured by sclerotic cortical bone or in cases of intra-articular lesions, where bone deposition from the intracapsular periosteum is usually less.12,13 In addition, intramedullary-located osteoid osteomas may not exhibit surrounding bone sclerosis.14 Indirect manifestations of synovial inflammation and joint effusion may be evident, or symptoms that mimic osteoarthritis may be present.13,15 When treatment is delayed, secondary osteopenia and changes in bone morphology may be observed.11 If the nidus is larger than 1.5 cm, the lesion is usually designated as an osteoblastoma.16,17 Osteoblastomas are seen radiologically as lesions with a lucent, slow-growing, expansile area with irregular sclerosis and no definite nidus.18

An 11-year-old girl presented with chronic midtibial pain and localized warmth on examination. Lateral radiograph showing diffuse anterior cortical thickening (arrow) centered on a subtle lucency, which was diagnosed as an osteoid osteoma (A). Axial proton-density fat-saturated magnetic resonance image showing diffuse high-signal medullary edema and periostitis surrounding a markedly thickened low-signal cortex, within which a 3-mm osteoid osteoma lies (B). Axial computed tomography scan obtained during radiofrequency ablation showing the densely thickened cortex and an ablation needle completely occupying the nidus (C).

Figure 1:

An 11-year-old girl presented with chronic midtibial pain and localized warmth on examination. Lateral radiograph showing diffuse anterior cortical thickening (arrow) centered on a subtle lucency, which was diagnosed as an osteoid osteoma (A). Axial proton-density fat-saturated magnetic resonance image showing diffuse high-signal medullary edema and periostitis surrounding a markedly thickened low-signal cortex, within which a 3-mm osteoid osteoma lies (B). Axial computed tomography scan obtained during radiofrequency ablation showing the densely thickened cortex and an ablation needle completely occupying the nidus (C).

Computed Tomography

The most common appearance of osteoid osteoma on computed tomography (CT) is as a small, well-delineated, low-attenuation nidus surrounded by a dense sclerotic reaction (Figure 2). Foci of calcification may be visible. A recently described CT finding is the presence of fine, linear, low-density vascular channels that can surround osteoid osteomas. When present, such vascular grooves have high sensitivity and specificity in the diagnosis of osteoid osteoma.19

A 23-year-old man presented after 18 months of knee pain due to medullary osteoid osteoma. Axial computed tomography scan from a treatment planning study showing the lucent osteoid osteoma, subtle central calcification, and surrounding medullary sclerosis. Note the vascular channel entering the medial aspect of the lesion (A). Coronal proton-density fat-saturated magnetic resonance image showing a zone of marrow edema centered on a high-signal nidus adjacent to the physeal scar (B).

Figure 2:

A 23-year-old man presented after 18 months of knee pain due to medullary osteoid osteoma. Axial computed tomography scan from a treatment planning study showing the lucent osteoid osteoma, subtle central calcification, and surrounding medullary sclerosis. Note the vascular channel entering the medial aspect of the lesion (A). Coronal proton-density fat-saturated magnetic resonance image showing a zone of marrow edema centered on a high-signal nidus adjacent to the physeal scar (B).

A CT scan is useful in diagnosing intra- or juxta-articular osteoid osteomas, and it has been proposed that CT must be used in all patients with suspected osteoid osteomas because it has better diagnostic accuracy compared with plain radiographs or magnetic resonance imaging in these cases.20,21 Preoperative localization of osteoid osteomas can be facilitated using CT guidance.22,23 Percutaneous ablation of lesions under CT guidance is well established and is discussed later (Figure 3).24–28 Computed tomography–guided ablation of osteoid osteomas has also been described in technically challenging locations, such as the spine.29,30

An 11-year-old boy presented with an osteoid osteoma in the right medial femoral neck that was treated with radiofrequency ablation. Computed tomography (CT) scanogram image showing the lucent osteoid osteoma surrounded by medullary sclerosis and overlying cortical thickening. An ablation needle has been placed in the lesion under CT guidance (A). Axial CT scan showing the needle traversing the osteoid osteoma. A lateral approach was used to avoid the grossly thickened cortical bone (B).

Figure 3:

An 11-year-old boy presented with an osteoid osteoma in the right medial femoral neck that was treated with radiofrequency ablation. Computed tomography (CT) scanogram image showing the lucent osteoid osteoma surrounded by medullary sclerosis and overlying cortical thickening. An ablation needle has been placed in the lesion under CT guidance (A). Axial CT scan showing the needle traversing the osteoid osteoma. A lateral approach was used to avoid the grossly thickened cortical bone (B).

Bone Scintigraphy

Due to the correlation between osteoblastic activity and the intensity of radiopharmaceutical uptake, bone scintigraphy usually shows intense uptake in the arterial phase within the richly vascular nidus and in the delayed phase within surrounding reactive bone (Figure 4).31 Usually, an intense area of radiotracer uptake is found in the region of the nidus and less in the reactive bone. This pattern, which is known as the double-density sign, is diagnostic of osteoid osteoma.32 The area of uptake may be wide. Historically, a pinhole collimator has been used to demonstrate the nidus because the reactive bone uptake may obscure it.14

A 16-year-old boy presented with a 1-year history of knee pain but normal clinical examination. Radionuclide bone scan image showing a wide zone of increased uptake in the proximal tibia due to increased osteoblastic activity provoked by an osteoid osteoma.

Figure 4:

A 16-year-old boy presented with a 1-year history of knee pain but normal clinical examination. Radionuclide bone scan image showing a wide zone of increased uptake in the proximal tibia due to increased osteoblastic activity provoked by an osteoid osteoma.

In children, increased uptake by active growth plates can obscure an adjacent osteoid osteoma. In this situation, comparison with the contralateral unaffected site is helpful to identify the tumor.13 In situations where radiofrequency ablation is not available, intraoperative radionucleotide imaging may be used to confirm complete resection of the tumor.14,33

Single-photon Emission Computed Tomography

Although in most cases a conventional bone scan followed by thin-section CT scan is sufficient, single-photon emission computed tomography (SPECT) can be helpful in diagnosing osteoid osteomas in cases in which bone scintigraphy uptake is subtle.34 A SPECT scan can detect smaller lesions by improved spatial resolution of overlying normal tissue uptake and has been advocated as helpful in depicting osteoid osteomas of the spine.14,35 Transaxial anatomic imaging of SPECT can further enhance its diagnostic ability in positioning suspicious lesions.36

Magnetic Resonance Imaging

The appearance of osteoid osteoma is variable with magnetic resonance imaging (MRI). A primarily cellular nidus will demonstrate low to intermediate signal intensity on T1-weighted images that increases on T2-weighted images (Figure 1B). A heavily calcified nidus appears as low to intermediate signal intensity on both T1- and T2-weighted images.37 A more striking finding is the presence of surrounding bone marrow edema or periostitis, best demonstrated on fluid-sensitive sequences (Figure 2B). Areas of densely sclerotic medullary or cortical bone may retain low signal intensity on all sequences. In some cases, the bone marrow and soft tissue edema is florid and can mimic an aggressive process, such as infection or malignancy. Reactive soft tissue mass with myxomatous change, cell-depleted juxtanidal bone marrow, and proteinaceous material may be confused with those of a malignant tumor or osteomyelitis.38,39

It has been suggested that MRI must not be interpreted without reference to plain radiographs and CT scans because the appearance of osteoid osteomas on MRI can mimic that of an aggressive lesion.25 Correlation with clinical information is the most important aspect of diagnosing osteoid osteomas. Following intravenous gadopentate dimeglumine, both the central nidus and surrounding edema show enhancement. This technique is not always necessary, but occasionally it may assist the differential diagnosis along with other modalities.

Sonography

Historically, the use of preoperative Doppler duplex color localization of osteoid osteomas has been reported as a means of assessment of the vascularity of the nidus or the nidus’ feeding artery.40 Color Doppler sonography may show increased blood supply and demonstrate the entering vessel at the site of the lesion.41 Sonography is limited by its inability to penetrate bone and has been replaced by other imaging modalities.

Histopathology

Osteoid osteomas consist of a nidus that is surrounded by sclerotic bone, the density of which usually varies with time from the onset of the lesion.42 Macroscopically, the nidus is a distinct round or oval reddish area with little contact with its surrounding sclerotic bone. Depending on the degree of calcification, the nidus’ consistency may vary from soft and granular to hard and sclerotic. Older lesions demonstrate formation of defined trabeculae.

Intraoperatively, the tumor can be visualized protruding from the bone surface, or it may be hidden under a thick cortical layer of hyperostotic reactive bone. Intracortical and subperiosteal lesions are often associated with hyperemia and edema of the surrounding soft tissues.4 In tubular bones specifically, osteoid osteomas that present subperiosteally tend to become intracortical due to continuous bone remodeling and subperiosteal new bone apposition.43

Histologically, the nidus appears as a small, well-defined area consisting of interlacing, irregular bone trabeculae of varying mineralization (Figure 5). Size, thickness, and mineralization diversity of trabeculae are evident among different lesions, as well as in different areas of the same lesion. The nidus may demonstrate a zonal arrangement of trabecular architecture, with the central part being more sclerotic and the periphery less mineralized and with more cells. Osteoid trabeculae are surrounded mainly by osteoblasts.44

Hematoxylin-eosin stain (original magnification ×200) showing trabeculae of woven bone lined by osteoblasts surrounded by a loose vascular connective tissue stroma.

Figure 5:

Hematoxylin-eosin stain (original magnification ×200) showing trabeculae of woven bone lined by osteoblasts surrounded by a loose vascular connective tissue stroma.

Osteoclast-like, multinucleated giant cells have also been reported to be present.45 A reactive bone-formation zone with thickened trabeculae and a loose fibro-vascular stroma surrounds the nidus. The surrounding zones of soft tissue, skeletal muscle, and bone show increased vascularity, with vessels becoming smaller closer to the nidus.46 In chronic lesions, the fibro-vascular stroma may be dense with chronic inflammatory cell infiltration.

Pain commonly induced by osteoid osteomas is attributed to unmyelinated nerve fibers found within the nidus.47 Immunohistochemical analysis has detected peripheral nerve fibers in the reactive zone and the nidus, with the greatest number being at the interface between the reactive zone and the edge of the nidus.44 Increased local concentration of prostaglandins (PGE2, PGI2, PGF2-alpha) and increased urinary excretion of 6-keto-PGF1 (the major urinary metabolite of PGI2) have been discussed in the literature in cases of osteoid osteoma.48,49 Pain mediated by prostaglandins has been attributed to the vasodilatory and vascular proliferation effect causing increased local pressure and thus stimulating the peripheral nerve fibers of the reactive zone, or through activation of the bradykinin system.50 Increased prostaglandin values are reversible after osteoma removal.49 Although the remodeling and osteolytic effect of prostaglandins is still under consideration, prostaglandins of the E series stimulate osteoclastic bone resorption in vitro and may contribute to the formation of osteoid osteoma.51

Nidus osteoblasts also display strong diffuse staining for COX-2, a key enzyme in the production of prostaglandins and in particular of prostaglandin E2.52 This enzyme appears to be a major factor in osteoid osteoma pain, and inhibition of COX-2 production enables control of symptoms.53

Differential Diagnosis

The differentiation of osteoid osteomas from other benign bone-forming lesions is based on the difference in size, location, pathology, and clinical symptoms, pathology, and clinical symptoms.5 In particular, osteoblastomas are larger in size (usually more than 1.5 to 2 cm) and tend to expand instead of regress.45 Osteoblastomas are also painful but generally without characteristic night exacerbation seen with osteoid osteomas, and pain does not respond dramatically to salicylates or NSAIDs. Osteoblastomas have a predilection for vertebrae and can be accompanied more frequently with neurological symptoms or paravertebral muscle spasm.6,7 Instances of osteoid osteoma transition to osteoblastoma have been reported, although they are rare.54,55 Radiographically, osteoblastomas appear larger with less reactive sclerosis.5 Plain radiographs alone may not be distinctive enough to establish the diagnosis, and CT scans can give more information on the expansive nature of the lesion.

When small in size, a Brodie’s abscess may appear similar to an osteoid osteoma on plain radiographs.9 Imaging using MRI, CT, and scintigraphy can help differentiate between osteoid osteomas and osteomyelitis, as well as other types of tumors, including nonossifying fibromas, chondroblastomas, enchondromas, eosinophilic granulomas, and malignant bone tumors.32,39,56

In children, infantile cortical hyperostosis, osteomyelitis, Perthes’ disease, leg-length discrepancy, healing stress fractures, tuberculosis, and neuromuscular conditions should be considered.57 Imaging using CT, bone, and SPECT scans are useful in delineating the nature of the lesion. Patients with unexplained low-back pain and sciatic pain in the second decade of life should be carefully examined to rule out osteoid osteoma.58

Treatment

Moberg59 suggested that the natural history of osteoid osteoma is that of spontaneous healing. In various studies, it has been noted that if the osteoid osteoma is not excised, complete resolution of symptoms occurs within 6 to 15 years.42,59 Administering aspirin or other NSAIDs can reduce this time period to 2 to 3 years.50,53 Kneisl and Simon60 reported permanent relief of symptoms and regression of the nidus after prolonged NSAIDs treatment for 30 to 40 months. Strict selection criteria should be applied if nonoperative treatment is considered, given the potential side effects of prolonged NSAIDs administration. Nonoperative management should be considered in patients where osteoid osteoma is not easily accessible by surgery.

Various techniques have been described for the preoperative localization of osteoid osteomas, such as angiography and placing wires and needles dipped in methylene blue over the nidus while under CT guidance.23 Radioisotope imaging with scintimetric guidance for intraoperative localization and excision has been reported.61–63 Historically, in cases of intracortical lesions, preoperative oral tetracycline administration and examination of nidus’ fluorescence under ultraviolet light has been used to demonstrate the lesion and to verify excision, but such techniques are not currently considered practical.64,65

Osteoid osteoma was traditionally treated with excision of the nidus.6,16 Although the nidus needs to be removed completely to achieve symptomatic relief, complete removal of the sclerotic bone is not necessary. A well-planned surgical approach is essential. Radiographs or CT scans confirm identification of the nidus before and after en bloc removal, and then the nidus undergoes histological examination for confirmation. En bloc resection has the disadvantages of a large surgical exposure and excision of a large part of sclerotic bone. Bone grafting or internal fixation may be necessary, depending on the size of the bone defect left by the resection.5 Unroofing and curettage has a role in structurally critical locations, such as the neck of femur because the central sclerotic structure is not disrupted.4 Multiple articles report arthroscopic removal of intra-articular osteoid osteomas.66–69

Several methods have been described whereby osteoid osteomas may be treated percutaneously using CT guidance. These include trephine excision, cryoablation, radiofrequency ablation, and laser thermocoagulation.24–28 The use of 3-dimensional C-arm radiographs during percutaneous excision in the long bones of children has also been reported.70 However, most patients in the literature undergoing percutaneous ablation or resection required general anesthesia for pain control. The need for a general anesthetic increases the invasive nature and the cost of these procedures and reduces the advantages of percutaneous treatment over surgical resection. Furthermore, these techniques require equipment not commonly available in all hospitals.

Fine drills, bone trephine, or Tru-Cut needles (Medline Industries, Inc, Mundelein, Illinois) have been described for use in precise and bone-sparing resection. With smaller instruments, the need for a general anesthetic is also reduced, and the procedure can be performed in the outpatient setting, reducing the overall cost. Roger et al26 reported 16 patients who were treated using percutaneous CT-guided excision and had satisfactory results in 14 patients. The 2 failures were attributed to the proximity of the lesion to the articular margin and excessive periosteal reaction preventing access. The authors concluded that intraoperative CT guidance and immediate postoperative scintigraphy were effective in localizing and confirming removal of the nidus in an outpatient setting.26 In a series of 38 patients, Sans et al71 reported a cure rate of 84% at 3.7 years postoperatively and 2 instances of femoral fracture at 2 months. Muscolo et al72 reported superior outcomes of CT-guided minimally invasive surgery rather than open surgery. Overall, percutaneous CT-guided procedures have profoundly modified the treatment of osteoid osteoma. Rosenthal et al73 reported a statistically significant reduction in hospital stay over the past 20 years by using more conservative and intralesional procedures.

Gangi et al74 reported laser interstitial photocoagulation as a successful minimally invasive procedure. In their case series of 114 patients, 112 patients had a visual analog score of 0 at 1 week postoperatively. Six patients had recurrence and were successfully treated at the second attempt.74 A recent retrospective study reported 26 patients treated by percutaneous trephine resection and 100 by percutaneous interstitial laser ablation.75 Percutaneous trephine resection had a success rate of 95% at 24 months. Two patients sustained skin burns and 1 reported meralgia. Interstitial laser ablation had a success rate of 94% at 24 months, with complications including infection, tendonitis, hematoma, and common peroneal nerve injury. The outcome was worse regardless of treatment method in patients younger than 18 years and in instances where the nidus was 12 mm or larger.75

Percutaneous thermocoagulation of the nidus has been used by de Berg et al,76 who reported 17 patients treated successfully with this method. Percutaneous radiofrequency ablation has been proposed as an alternative to the operative treatment of osteoid osteomas.77 The newer technology radiofrequency probes allow thermocoagulation of a region as large as 5 cm using a single probe (Figure 1C). Generally, osteoid osteoma nidus size is up to 1 cm; consequently, the conventional monopolar radio frequency probe is adequate. A series of 21 patients with osteoid osteoma in atypical locations (eg, hip, radioulnar joint, phalanx) showed radiofrequency ablation to be successful, albeit with only short-term follow-up data available.78 A 5-year review of radiofrequency ablation confirmed cure in 38 of 39 patients, with 1 case of a broken drill and 1 of infection as the only reported complications.79 Similarly, a 5-year case series of 21 patients confirmed a primary cure rate of 89.6% that increased to 93% if a second treatment was required.80

With osteoid osteoma affecting the spine, the efficacy and safety of this procedure has been assessed, especially considering the effect of increased temperature in the spinal canal. Dupuy et al81 reported that this technique has no cytotoxic effects into the spinal canal, especially with internally cooled radiofrequency probes. Recently, Peyser et al82 and Neumann et al83 also concluded that CT-guided percutaneous radiofrequency ablation of osteoid osteomas is a safe, effective, and minimally invasive procedure with a high success rate and no recurrence. Rimondi et al84 reported a series of 557 patients and recommended modifications to electrode parameters, duration of ablation with regard to the size, and morphology of the lesion.

Recently, bipolar radiofrequency technology has gained interest in the management of osteoid osteoma. Some drawbacks of monopolar radiofrequency ablation include skin burns at the site of neutral electrode and aberrant currents causing irregular areas of necrosis or inducing heat at metallic implants.85 Another innovative approach with promising results, particularly for inaccessible lesions, has been described by Mylona et al,29 who successfully performed radiofrequency ablation using a probe needle with expandable electrodes. A retrospective review of 81 patients treated either by conventional surgery or minimally invasive techniques for osteoid osteoma of the spine found no difference in outcome.86

In its 2004 issue, the National Institute of Clinical Excellence stated that “Current evidence on the safety and efficacy of CT-guided thermocoagulation of osteoid osteoma appears adequate to support its use, provided that the normal arrangements are in place for consent, audit and clinical governance.”87

Regardless of the technique used, it is imperative that a biopsy be taken at the time of intervention to confirm the diagnosis. Various methods have been used to determine the complete removal of the nidus. These include immediate radiographs of the patient, tomogram or bone scan of the resected specimen, preoperative tetracycline labeling and use of intraoperative ultraviolet light, microradiography, specimen autoimaging on underdeveloped film, intraoperative use of bone scintigraphy, and immediate postoperative scintigraphy.26,65,88–92

Conclusion

Osteoid osteomas are the third most common benign bone tumor and have a wide variation in presentation. They tend to present in the second decade of life with pain that is worse at night and is relieved by salicylates. Plain radiographs and CT are the mainstays of imaging. Osteoid osteomas consist of a nidus with surrounding sclerotic bone. The natural history of an untreated osteoid osteoma is natural regression, which occurs within 6 to 15 years but can be reduced to 2 to 3 years with treatment with aspirin or NSAIDs.59

Various surgical techniques have been discussed in the literature. With the advancement of radiological techniques, percutaneous procedures with less morbidity have been introduced. Surgery is still performed in instances where the location of the lesion precludes percutaneous techniques. If a complete excision or ablation of the nidus is achieved, the reactive bone sclerosis regresses and patients become asymptomatic. In the future, identification of factors that control the local production of prostaglandins may lead to further treatment modalities.53

References

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