Orthopedics

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Review Article 

Clinicopathological Features, Diagnosis, and Treatment of Adamantinoma of the Long Bones

Panayiotis J. Papagelopoulos, MD, DSc; Andreas F. Mavrogenis, MD; Evanthia C. Galanis, MD; Olga D. Savvidou, MD; Carrie Y. Inwards; Franklin H. Sim, MD

Abstract

Adamantinoma of the long bones is a low-grade, slow-growing, primary malignant bone tumor composed of epithelial cells in a fibrous or osteofibrous stroma.1,2 It has a wide range of histological patterns.3-18 Despite the considerable range of each histologic pattern, most current studies have shown that long bone adamantinoma appears to be of an epithelial nature. The tibial lesion’s name comes from its somewhat similar histologic appearance to the more common odontogenic adamantinoma of the jaw bones.18,19 Despite the histological similarities there is no proof that these tumors have a similar histiogenetic origin.19

Long bone adamantinomas can be divided in two main groups with distinct histological and radiographic features. The first–classic adamantinoma–is characterized by an abundance of tumor cells and a destructive growth pattern. The second, differentiated adamantinoma, is characterized histologically by a predominance of an osteofibrous dysplasia-like pattern with a small, inconspicuous component of epithelial tumor elements.12,18,19 Radiographically, classic adamantinomas are either intracortical or associated with complete cortical disruption, intramedullary involvement, and expansion beyond the periosteum into adjacent soft tissues, while differentiated adamantinomas are intracortical and often multicentric lesions.12,19,20

This article discusses the epidemiology, clinicopathological and imaging features, diagnosis, treatment, and prognosis of adamantinoma of the long bones.

Adamantinoma of the long bones is a rare tumor that accounts for 0.3%-1% of all malignant bone tumors.4-9,21 In 1986, Moon and Mori2 performed a meta-analysis of 200 cases. In 1996, Unni18 reported 36 cases in an analysis of 5641 primary malignant bone tumors from a single institution.

The literature suggests a slight male predominance.1,2,4-9,21 Adamantinomas usually are diagnosed after skeletal maturity. Although 75% of the cases occur between the second and third decades of life,18 adamantinomas have also been reported in older patients, as well as in children aged <14 years.18,22,23 Differentiated adamantinomas tend to occur in younger patients.18,19

More than 90% of adamantinomas appear in the tibia, with fibular involvement coexisting in 50% of the cases.12,18,19 The tumor usually is located in the diaphysis and, less frequently, the tibial metaphysis. Rare cases of adamantinomas of the olecranon, the ribs, the radius, the spine, the metatarsus, and the humerus also have been reported.24-31

Figure 1: AP (A) and lateral (B) plain radiographs show an expansile mixed lytic and sclerotic lesion of the mid-portion of the right tibia.

A history of previous trauma or fracture occurring months or years prior to the onset of symptoms is reported in approximately 60% of patients. The most common presentation is of a gradually evolving mass associated with dull, insidious, aching pain. Bowing deformity of the tibia and pathologic fractures may occur. Advanced or recurrent lesions may be associated with soft-tissue involvement.12,18,21 Severe paraneoplastic, humorally mediated hypercalcaemia, hypercalcaemic coma, and pancreatitis have been reported.32-35

Radiographically, adamantinoma usually appears as a mixed lytic and sclerotic central lesion or multiple, sharply circumscribed lucencies with sclerosis of the intervening bone (Figure 1). This slowly growing, expansile tumor eventually causes endosteal scalloping and thinning, interruption, or destruction of the cortex without periosteal reaction. Moderate to severe anterior bowing deformity is common.19,20 Classical adamantinoma usually is intracortical with evidence of complete cortical disruption and intramedullary and soft-tissue involvement. Involvement of the anterolateral cortex of the tibia with multiple lucencies and sclerotic foci characterizes differentiated adamantinoma. These imaging features may be similar to those observed in osteofibrous dysplasia.12,18,20

Technetium pyrophosphate bone scan shows intense increased uptake tracer accumulation, corresponding closely to the extent of the lesion.18,21,36 In addition, bone scan may show a coexisting fibular involvement.

Computed tomography reveals an osteolytic lesion with expansion and destruction of the cortex (Figure 2), and probable extension to the surrounding soft tissues.21,37 Magnetic resonance imaging…

Adamantinoma of the long bones is a low-grade, slow-growing, primary malignant bone tumor composed of epithelial cells in a fibrous or osteofibrous stroma.1,2 It has a wide range of histological patterns.3-18 Despite the considerable range of each histologic pattern, most current studies have shown that long bone adamantinoma appears to be of an epithelial nature. The tibial lesion’s name comes from its somewhat similar histologic appearance to the more common odontogenic adamantinoma of the jaw bones.18,19 Despite the histological similarities there is no proof that these tumors have a similar histiogenetic origin.19

Long bone adamantinomas can be divided in two main groups with distinct histological and radiographic features. The first–classic adamantinoma–is characterized by an abundance of tumor cells and a destructive growth pattern. The second, differentiated adamantinoma, is characterized histologically by a predominance of an osteofibrous dysplasia-like pattern with a small, inconspicuous component of epithelial tumor elements.12,18,19 Radiographically, classic adamantinomas are either intracortical or associated with complete cortical disruption, intramedullary involvement, and expansion beyond the periosteum into adjacent soft tissues, while differentiated adamantinomas are intracortical and often multicentric lesions.12,19,20

This article discusses the epidemiology, clinicopathological and imaging features, diagnosis, treatment, and prognosis of adamantinoma of the long bones.

Epidemiological Data

Adamantinoma of the long bones is a rare tumor that accounts for 0.3%-1% of all malignant bone tumors.4-9,21 In 1986, Moon and Mori2 performed a meta-analysis of 200 cases. In 1996, Unni18 reported 36 cases in an analysis of 5641 primary malignant bone tumors from a single institution.

The literature suggests a slight male predominance.1,2,4-9,21 Adamantinomas usually are diagnosed after skeletal maturity. Although 75% of the cases occur between the second and third decades of life,18 adamantinomas have also been reported in older patients, as well as in children aged <14 years.18,22,23 Differentiated adamantinomas tend to occur in younger patients.18,19

More than 90% of adamantinomas appear in the tibia, with fibular involvement coexisting in 50% of the cases.12,18,19 The tumor usually is located in the diaphysis and, less frequently, the tibial metaphysis. Rare cases of adamantinomas of the olecranon, the ribs, the radius, the spine, the metatarsus, and the humerus also have been reported.24-31

Clinical Manifestations

 

Figure 1A: Expansile mixed lytic and sclerotic lesion of the mid-portion of the right tibia

Figure 1B: Expansile mixed lytic and sclerotic lesion of the mid-portion of the right tibia

Figure 1: AP (A) and lateral (B) plain radiographs show an expansile mixed lytic and sclerotic lesion of the mid-portion of the right tibia.

A history of previous trauma or fracture occurring months or years prior to the onset of symptoms is reported in approximately 60% of patients. The most common presentation is of a gradually evolving mass associated with dull, insidious, aching pain. Bowing deformity of the tibia and pathologic fractures may occur. Advanced or recurrent lesions may be associated with soft-tissue involvement.12,18,21 Severe paraneoplastic, humorally mediated hypercalcaemia, hypercalcaemic coma, and pancreatitis have been reported.32-35

Imaging Features

Radiographically, adamantinoma usually appears as a mixed lytic and sclerotic central lesion or multiple, sharply circumscribed lucencies with sclerosis of the intervening bone (Figure 1). This slowly growing, expansile tumor eventually causes endosteal scalloping and thinning, interruption, or destruction of the cortex without periosteal reaction. Moderate to severe anterior bowing deformity is common.19,20 Classical adamantinoma usually is intracortical with evidence of complete cortical disruption and intramedullary and soft-tissue involvement. Involvement of the anterolateral cortex of the tibia with multiple lucencies and sclerotic foci characterizes differentiated adamantinoma. These imaging features may be similar to those observed in osteofibrous dysplasia.12,18,20

Technetium pyrophosphate bone scan shows intense increased uptake tracer accumulation, corresponding closely to the extent of the lesion.18,21,36 In addition, bone scan may show a coexisting fibular involvement.

Computed tomography reveals an osteolytic lesion with expansion and destruction of the cortex (Figure 2), and probable extension to the surrounding soft tissues.21,37 Magnetic resonance imaging (MRI) is useful in providing information concerning the intramedullary and soft-tissue extent of the tumor.9,20,36-38 On T1-weighted MRI, the lesion has a low intensity signal, whereas on T2-weighted MRI the signal is much brighter and does not diminish with the fat suppression technique.

In a study of 22 patients, two morphologic patterns were distinguished in MRI: a solitary, lobulated focus versus a pattern of multiple small modules in one or more foci; however, these characteristics were not related to the histologic subtype.38

Figure 2: CT scan of the right leg shows a lytic expansile lesion within the tibia

Figure 2: CT scan of the right leg shows a lytic expansile lesion within the tibia. There is intramedullary involvement with some calcifications and thinning of the cortex, particularly posteriorly.

Histologic Features

Histologically, adamantinoma is composed of epithelial islands in a spindle cell stroma. The relative amounts of the two components can vary considerably (Figure 3). Several histologic variants have been described corresponding to a variety of different epithelial cell patterns that can be found. Therefore, this range of morphologic patterns can mimic many primary or metastatic bone lesions.21,39 A number of immunohistochemical and electron microscopic studies have shown adamantinoma to be of epithelial derivation.1,9-11,36,40-44 In some tumors the stromal component has a fibrous dysplsia-like appearance with or without scattered spicules of woven bone.18,19

Figure 3A: Low-power view shows islands of epithelial cells surrounded by fibrous tissue

Figure 3B: High-power view of the cluster of epithelial cells within the fibrous stroma

Figure 3: Histological appearance of adamantinoma. Low-power view (A) shows islands of epithelial cells surrounded by fibrous tissue and high-power view (B) of the cluster of epithelial cells within the fibrous stroma.

Differential Diagnosis

Because of its rarity and differing histological patterns, adamantinoma histologically may resemble epithelial metastasis, hemangioendothelioma, hemangiosarcoma, fibrous and osteofibrous dysplasia, nonossifying fibromas, and chondromyxoid fibromas.18,19,44-47 Clinical information such as patient age and history, as well as the location in the tibial diaphysis, may aid in diagnosis.

It is important to differentiate adamantinoma from osteofibrous dysplasia.20 Adamantinoma generally is painful, is observed during adulthood, has different radiographic features, is progressive during adult age, and may expand into the soft tissues. However, osteofibrous dysplasia seldom progresses during childhood, and any progression of the lesion stops after puberty. Exceptional cases have been reported of adamantinoma that began during childhood and have radiographic features similar to osteofibrous dysplasia.45-47

Adamantinoma must be suspected if a tibial lesion becomes painful or if it grows after puberty. In such cases, extensive biopsy from the most radiolucent areas is recommended. However, given the heterogeneity of the histology within different areas of adamantinomas, sampling errors are possible with limited biopsy specimens. These errors have led to reclassification of these tumors from osteofibrous dysplasia to adamantinoma after repeat biopsy with adequate tissue.45-47

 

Figure 4A: AP plain radiograph after wide resection of the tumor

Figure 4B: Llateral plain radiographs after wide resection of the tumor

Figure 4: AP (A) and lateral (B) plain radiographs after wide resection of the tumor and reconstruction using a 13 cm intercalary tibial allograft fixed using a DCP plate and screws and autologous iliac bone grafting at the host bone allograft junction.

Treatment and Prognosis

Owing to the rarity of adamantinomas, data is insufficient concerning the safest and most effective treatment modality. These tumors are of low-grade malignancy and highly radioresistant.48,49 Thus surgery is the treatment of choice. Although limited experience with them has been reported, chemotherapy and radiation therapy have not been shown to be effective.8

Operative treatment includes either surgical resection with wide margins and reconstruction of the segmental defect,4,5,8,9,12,18,21,50-52 or amputation.1,2,5,9 Limb reconstruction options include the use of allografts (intercalary, osteoarticular, or morselized), vascularized and nonvascularized fibular autografts, metallic segmental implants, and distraction osteogenesis.9,21,51,53 Intercalary reconstruction appears to be the most successful method (Figure 4). Qureshi et al9 reported a limb salvage rate of 84%. They used allografts in 61% of the reconstructions after resection of adamantinomas of long bones. The majority were intercalary reconstructions. No differences in the efficacy of different fixation techniques were noted. Complications related to the reconstruction were unacceptably high (48% of patients), including nonunion (24%) and fracture of the allograft (23%). Vascularized fibular grafts have been considered the best type of graft for large segmental bone defects after bone tumor resections.54,55

Local recurrence is common in inadequately treated patients.12,21,56,57 Wide operative margins are associated with a lower rate of local recurrence than marginal or intralesional margins.8,9,24 However, a 18.6% rate of local recurrence at 10 years has been reported after wide-margin surgical excision of adamantinomas.9 Local recurrences usually occur 5 to 15 years after primary excision of the tumor. Late local recurrences have been reported at 24 and 36 years after diagnosis.21,56 No statistically significant difference between local recurrence rate and tumor stage, duration of symptoms, patient gender and age, type of biopsy, and type of grafting has been documented.9,12 Wide resection is also indicated for recurrent tumors.56

The near-benign biology and slow-growing nature of adamantinoma are reflected in the good survival rates even after local recurrences and lung or regional lymph node metastases.21,39,51 Late metastases may occur in 10%-30% of patients with adamantinomas, most frequently in the lungs, the regional lymph nodes, or the bones.19,21,24,32-35 After wide margin surgical excision of the tumor or amputation, overall 10-year survival rates vary from 82% to 87%.1,2,8,12

Conclusion

Adamantinoma of the long bones is a rare, primary, low-grade, slow-growing malignant bone tumor. It is expressed with a wide range of histological patterns. Histologically, the tumor is composed of an epithelial component surrounded by a fibrous stroma that may or may not contain spicules of woven bone. In the majority of cases, adamantinomas are located in the tibial diaphysis. Limb salvage with wide surgical resection and reconstruction or amputation is the most effective treatment. Local recurrence is associated with incomplete resection. Survival rates range from 82% to 87%. Late metastases, mainly to the lungs, may occur.

References

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Authors

Drs Papagelopoulos and Mavrogenis are from the First Department of Orthopedic Surgery, Athens University Medical School, Athens, Greece, Dr Galanis is from the Division of Medical Oncology, Mayo College of Medicine, Rochester, Minn, Dr Savvidou is from the Department of Orthopedics, Thriasion General Hospital, Elefsis, Hellas-Greece, Ms Inwards is from the Division of Anatomic Pathology, Mayo College of Medicine, Rochester, Minn, and Dr Sim is from the Department of Orthopedic Surgery, Mayo College of Medicine, Rochester, Minn.

Drs Papagelopoulos, Mavrogenis, Galanis, Savvidou, and Sim and Ms Inwards have no industry relationship to declare.

The material presented at or in any Vindico Medical Education continuing education activity does not necessarily reflect the views and opinions of Vindico Medical Education or Orthopedics. Neither Vindico Medical Education or Orthopedics, nor the faculty endorse or recommend any techniques, commercial products, or manufacturers. The faculty/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 utilizing any product.

Correspondence should be addressed to: Panayiotis J. Papagelopoulos, MD, DSc, Athens University Medical School, 4 Christovassili Street, Neo Psychikon, 15451, Athens, Greece.

10.3928/01477447-20070301-04

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