Fibrous cortical defect (historical)
Updates to Article Attributes
Fibrous cortical defects (FCD) are benign bony lesions, and are a type of fibroxanthoma, histologically identical to the larger non-ossifying fibroma (NOF).
Epidemiology
Fibrous cortical defects typically occur in children (usually 2-15 years), and indeed are one of the most common benign bony lesions, which combined with non-ossifying fibromas are seen in up to 40% of skeletally immature children/adolescents 3. There is a male predilection by a ratio of 2:1 3.
Clinical presentation
They are asymptomatic and self limiting-limiting, completely healing by adulthood.
Pathology
FIbrousFibrous cortical defects macroscopically appear as fleshy, fibrous, yellow or tan-brown lesions with variable areas of hemorrhage 3.
Microscopic examination reveals the lesions to be highly cellular containing spindle-shaped cells on a background of stromal tissue in a prominent storiform pattern. Foamy histiocytes, and multi-nucleatedmultinucleated giant cells are also seen. Mitotic figures and/or cellular dysplasia should not be seen 3.
During the healing phase, there is an increase in osteoblastic activity as new bone replaces the defect is replaced by new bone, gradually being remodelled and completely disappearing 2.
Radiographic features
FCDs are a benign lytic bone lesions, and, along with fibrous dysplasia shares the F in the popular mnemonic FEGNOMASHIC.
They typically occur withinin the metaphysis or diametaphyseal junction and appear as small (<2-3 cm) lucent defects within the cortex that over time become sclerotic as they heal. They are typically located in the distal femur or proximal or distal tibia. They are much less frequently seen in the upper limb 2-3.
Importantly, there is no associated soft tissue mass 3.
Plain filmRadiography and CT
- lucent intracortical defects
- outlined by a thin rim of sclerosis
- no involvement of the underlying medullary cavity
- no periosteal reaction
MRI
Signal characteristics include:
- T1: hypointense
- T2: variable, depending on the phase of healing 3
Nuclear medicine (bone scan)
Appearance depends on phase of the lesion. In general they are negative, however, mild hyperaemia and moderate bone uptake are present during healing. If extensive uptake or hyperaemia are present, then an alternative diagnosis or superimposed fracture should be considered 3.
Treatment and prognosis
As these lesions are benign, characteristic in appearance and self limiting-limiting, no treatment, biopsy or even follow-up is required in typical cases. If associated with pathological fracture (more common in NOF) then cast immobilization until the fracture has healed, followed by biopsy with or without curettage, and bone grafting may be necessary 3.
Differential diagnosis
- non-ossifying fibroma (NOF): larger (>2-3 cm), bubbly
- cortical desmoid: posteromedial aspect of the distal femur
- osteoid osteoma
- intracortical abscess
- stress fracture
- intracortical osteosarcoma
-<p><strong>Fibrous cortical defects (FCD)</strong> are benign bony lesions, and are a type of <a href="/articles/fibroxanthoma-of-bone">fibroxanthoma</a>, histologically identical to the larger <a href="/articles/non-ossifying-fibroma-1">non-ossifying fibroma (NOF)</a>.</p><h4>Epidemiology</h4><p>Fibrous cortical defects typically occur in children (usually 2-15 years), and indeed are one of the most common benign bony lesions, which combined with non-ossifying fibromas are seen in up to 40% of skeletally immature children/adolescents <sup>3</sup>. There is a male predilection by a ratio of 2:1 <sup>3</sup>.</p><h4>Clinical presentation</h4><p>They are asymptomatic and self limiting, completely healing by adulthood.</p><h4>Pathology</h4><p>FIbrous cortical defects macroscopically appear as fleshy, fibrous, yellow or tan-brown lesions with variable areas of hemorrhage <sup>3</sup>. </p><p>Microscopic examination reveals the lesions to be highly cellular containing spindle-shaped cells on a background of stromal tissue in a prominent storiform pattern. Foamy histiocytes, and multi-nucleated giant cells are also seen. Mitotic figures and/or cellular dysplasia should not be seen <sup>3</sup>.</p><p>During the healing phase, there is an increase in osteoblastic activity as the defect is replaced by new bone, gradually being remodelled and completely disappearing <sup>2</sup>. </p><h4>Radiographic features</h4><p>FCDs are a <a href="/articles/benign-lytic-bone-lesions">benign lytic bone lesions</a>, and, along with <a href="/articles/fibrous-dysplasia">fibrous dysplasia</a> shares the <strong>F</strong> in the popular mnemonic <a href="/articles/lytic-bone-lesion-mnemonic">FEGNOMASHIC</a>. </p><p>They typically occur within the metaphysis or diametaphyseal junction and appear as small (<2-3 cm) lucent defects within the cortex that over time become sclerotic as they heal. They are typically located in the distal femur or proximal or distal tibia. They are much less frequently seen in the upper limb <sup>2-3</sup>.</p><p>Importantly, there is no associated soft tissue mass <sup>3</sup>.</p><h5>Plain film and CT</h5><ul>- +<p><strong>Fibrous cortical defects (FCD)</strong> are benign bony lesions and are a type of <a href="/articles/fibroxanthoma-of-bone">fibroxanthoma</a>, histologically identical to the larger <a href="/articles/non-ossifying-fibroma-1">non-ossifying fibroma (NOF)</a>.</p><h4>Epidemiology</h4><p>Fibrous cortical defects typically occur in children (usually 2-15 years), and indeed are one of the most common benign bony lesions, which combined with non-ossifying fibromas are seen in up to 40% of skeletally immature children/adolescents <sup>3</sup>. There is a male predilection by a ratio of 2:1 <sup>3</sup>.</p><h4>Clinical presentation</h4><p>They are asymptomatic and self-limiting, completely healing by adulthood.</p><h4>Pathology</h4><p>Fibrous cortical defects macroscopically appear as fleshy, fibrous, yellow or tan-brown lesions with variable areas of hemorrhage <sup>3</sup>. </p><p>Microscopic examination reveals the lesions to be highly cellular containing spindle-shaped cells on a background of stromal tissue in a prominent storiform pattern. Foamy histiocytes and multinucleated giant cells are also seen. Mitotic figures and/or cellular dysplasia should not be seen <sup>3</sup>.</p><p>During the healing phase, there is an increase in osteoblastic activity as new bone replaces the defect, gradually being remodelled and completely disappearing <sup>2</sup>. </p><h4>Radiographic features</h4><p>FCDs are a <a href="/articles/benign-lytic-bone-lesions">benign lytic bone lesions</a>, and, along with <a href="/articles/fibrous-dysplasia">fibrous dysplasia</a> shares the <strong>F</strong> in the popular mnemonic <a href="/articles/lytic-bone-lesion-mnemonic">FEGNOMASHIC</a>. </p><p>They typically occur in the metaphysis or diametaphyseal junction and appear as small (<2-3 cm) lucent defects within the cortex that over time become sclerotic as they heal. They are typically located in the distal femur or proximal or distal tibia. They are much less frequently seen in the upper limb <sup>2-3</sup>.</p><p>Importantly, there is no associated soft tissue mass <sup>3</sup>.</p><h5>Radiography and CT</h5><ul>
-</ul><h5>Nuclear medicine (bone scan)</h5><p>Appearance depends on phase of lesion. In general they are negative, however mild hyperaemia and moderate bone uptake are present during healing. If extensive uptake or hyperaemia are present then an alternative diagnosis or superimposed fracture should be considered <sup>3</sup>.</p><h4>Treatment and prognosis</h4><p>As these lesions are benign, characteristic in appearance and self limiting, no treatment, biopsy or even follow-up is required in typical cases. If associated with pathological fracture (more common in NOF) then cast immobilization until the fracture has healed, followed by biopsy with or without curettage, and bone grafting may be necessary <sup>3</sup>.</p><h4>Differential diagnosis</h4><ul>- +</ul><h5>Nuclear medicine (bone scan)</h5><p>Appearance depends on phase of the lesion. In general they are negative, however, mild hyperaemia and moderate bone uptake are present during healing. If extensive uptake or hyperaemia are present, then an alternative diagnosis or superimposed fracture should be considered <sup>3</sup>.</p><h4>Treatment and prognosis</h4><p>As these lesions are benign, characteristic in appearance and self-limiting, no treatment, biopsy or even follow-up is required in typical cases. If associated with pathological fracture (more common in NOF) then cast immobilization until the fracture has healed, followed by biopsy with or without curettage, and bone grafting may be necessary <sup>3</sup>.</p><h4>Differential diagnosis</h4><ul>
-<a href="/articles/cortical-desmoid">cortical desmoid</a>: posteromedial aspect of distal femur</li>- +<a href="/articles/cortical-desmoid">cortical desmoid</a>: posteromedial aspect of the distal femur</li>