Fibrous cortical defect (historical)
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Fibrous cortical defects (FCD) are benign bone lesions histologically identicalis a previously used term to describe non-ossifying fibromas smaller than 2-3 cm. Non-ossifying fibroma is now the recommended term per the WHO classification of soft tissue and bone tumours (5th edition)6.
In the popular mnemonic for lucent bone lesions FEGNOMASHIC, non-ossifying fibroma accounts for the "N" and FCD can be considered to account for the "F".
Terminology
The term 'fibrousfibrous cortical defect' has been used for bone lesions representing non-ossifying fibromas smaller than 2-3 cm. According to the WHO classification of soft tissue and bone tumours (5th edition) the, the term is no longer recommended and instead, non-ossifying fibroma (NOF) is preferred 6.
Epidemiology
Fibrous cortical defects typically occur in children (usually 2-15 years), and are one of the most common benign bone 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, completely healing by adulthood.
Pathology
Fibrous cortical defects macroscopically appear as fleshy, fibrous, yellow or tan-brown lesions with variable areas of haemorrhage 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 multinucleated 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, gradually being remodelled and completely disappearing 4.
Radiographic features
Fibrous cortical defectsare benign lytic bone lesions, and, along with fibrous dysplasia share the F in the popular mnemonic FEGNOMASHIC.
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 3,4.
Importantly, there is no associated soft tissue mass 3.
Plain radiograph and CT
lucent intracortical defects
outlined by a thin rim of sclerosis
no involvement of the underlying medullary cavity
MRI
Signal characteristics include:
T1:
hypointensehypointenseT2:
variablevariable, depending on the phase of healing 3
Nuclear medicine (bone scan)
The appearance depends on the 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 is 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, no treatment, biopsy or follow-up is required in typical cases. If associated with pathological fracture (more common in non-ossifying fibromas) then cast immobilisation until the fracture has healed, followed by biopsy with or without curettage, and bone grafting may be necessary 3.
History and etymology
The fibrous cortical defect was first described by Dallas Burton Phemister (1882-1951) 5, an American orthopaedic surgeon in 1929 6.
Differential diagnosis
Possible differential considerations include
cortical desmoid:
posteromedialposteromedial aspect of the distal femurosteoid osteoma: night pains
-<p><strong>Fibrous cortical defects (FCD)</strong> are benign bone lesions histologically identical to <a href="/articles/non-ossifying-fibroma-1">non-ossifying fibromas</a>.</p><p>In the popular mnemonic for lucent bone lesions <a href="/articles/lucentlytic-bone-lesion-differential-diagnosis-mnemonic-1">FEGNOMASHIC</a>, non-ossifying fibroma accounts for the "N" and FCD can be considered to account for the "F".</p><h4>Terminology</h4><p>The term 'fibrous cortical defect' has been used for bone lesions representing non-ossifying fibromas smaller than 2-3 cm. According to the <a href="/articles/who-classification-of-tumors-of-bone">WHO classification of soft tissue and bone tumours (5th edition)</a> the term is no longer recommended and instead, <a href="/articles/non-ossifying-fibroma-1">non-ossifying fibroma (NOF)</a> is preferred <sup>6</sup>.</p><h4>Epidemiology</h4><p>Fibrous cortical defects typically occur in children (usually 2-15 years), and are one of the most common benign bone 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 haemorrhage <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>4</sup>. </p><h4>Radiographic features</h4><p>Fibrous cortical defects<strong> </strong>are <a href="/articles/benign-lytic-bone-lesions">benign lytic bone lesions</a>, and, along with <a href="/articles/fibrous-dysplasia">fibrous dysplasia</a> share the <strong>F</strong> in the popular mnemonic <a href="/articles/lucentlytic-bone-lesion-differential-diagnosis-mnemonic-1">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>3,4</sup>.</p><p>Importantly, there is no associated soft tissue mass <sup>3</sup>.</p><h5>Plain radiograph and CT</h5><ul>-<li><p>lucent intracortical defects</p></li>-<li><p>outlined by a thin rim of sclerosis</p></li>-<li><p>no involvement of the underlying medullary cavity</p></li>-<li><p>no <a href="/articles/periosteal-reaction">periosteal reaction</a></p></li>-</ul><h5>MRI</h5><p>Signal characteristics include:</p><ul>-<li><p><strong>T1:</strong> hypointense</p></li>-<li><p><strong>T2:</strong> variable, depending on the phase of healing <sup>3</sup></p></li>-</ul><h5>Nuclear medicine (bone scan)</h5><p>The appearance depends on the 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 is 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 follow-up is required in typical cases. If associated with pathological fracture (more common in non-ossifying fibromas) then cast immobilisation until the fracture has healed, followed by biopsy with or without curettage, and bone grafting may be necessary <sup>3</sup>.</p><h4>History and etymology</h4><p>The fibrous cortical defect was first described by <strong>Dallas Burton Phemister </strong>(1882-1951) <sup>5</sup>, an American orthopaedic surgeon in 1929 <sup>6</sup>.</p><h4>Differential diagnosis</h4><p>Possible differential considerations include</p><ul>-<li><p><a href="/articles/cortical-desmoid">cortical desmoid</a>: posteromedial aspect of the distal femur</p></li>-<li><p><a href="/articles/osteoid-osteoma">osteoid osteoma</a>: night pains</p></li>-<li><p><a href="/articles/osteomyelitis">osteomyelitis</a></p></li>-<li><p><a href="/articles/stress-fracture">stress fracture</a></p></li>-<li><p><a href="/articles/intracortical-osteosarcoma">intracortical osteosarcoma</a></p></li>- +<p><strong>Fibrous cortical defects (FCD)</strong> is a previously used term to describe <strong>non-ossifying fibromas</strong> smaller than 2-3 cm. <a href="/articles/non-ossifying-fibroma-1" title="Non-ossifying fibroma">Non-ossifying fibroma</a> is now the recommended term per the <a href="/articles/who-classification-of-tumors-of-bone">WHO classification of soft tissue and bone tumours (5th edition)</a> <sup>6</sup>.</p><p>In the popular mnemonic for lucent bone lesions <a href="/articles/lucentlytic-bone-lesion-differential-diagnosis-mnemonic-1">FEGNOMASHIC</a>, non-ossifying fibroma accounts for the "N" and FCD can be considered to account for the "F".</p><h4>Terminology</h4><p>The term <strong>fibrous cortical defect</strong> has been used for bone lesions representing non-ossifying fibromas smaller than 2-3 cm. According to the <a href="/articles/who-classification-of-tumors-of-bone">WHO classification of soft tissue and bone tumours (5th edition)</a>, the term is no longer recommended and instead, <a href="/articles/non-ossifying-fibroma-1">non-ossifying fibroma (NOF)</a> is preferred <sup>6</sup>.</p><h4>Epidemiology</h4><p>Fibrous cortical defects typically occur in children (usually 2-15 years) and are one of the most common benign bone 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 haemorrhage <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>4</sup>. </p><h4>Radiographic features</h4><p>Fibrous cortical defects<strong> </strong>are <a href="/articles/benign-lytic-bone-lesions">benign lytic bone lesions</a>, and, along with <a href="/articles/fibrous-dysplasia">fibrous dysplasia</a> share the <strong>F</strong> in the popular mnemonic <a href="/articles/lucentlytic-bone-lesion-differential-diagnosis-mnemonic-1">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>3,4</sup>.</p><p>Importantly, there is no associated soft tissue mass <sup>3</sup>.</p><h5>Plain radiograph and CT</h5><ul>
- +<li><p>lucent intracortical defects</p></li>
- +<li><p>outlined by a thin rim of sclerosis</p></li>
- +<li><p>no involvement of the underlying medullary cavity</p></li>
- +<li><p>no <a href="/articles/periosteal-reaction">periosteal reaction</a></p></li>
- +</ul><h5>MRI</h5><p>Signal characteristics include:</p><ul>
- +<li><p><strong>T1:</strong> hypointense</p></li>
- +<li><p><strong>T2:</strong> variable, depending on the phase of healing <sup>3</sup></p></li>
- +</ul><h5>Nuclear medicine (bone scan)</h5><p>The appearance depends on the 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 is 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 follow-up is required in typical cases. If associated with pathological fracture (more common in non-ossifying fibromas) then cast immobilisation until the fracture has healed, followed by biopsy with or without curettage, and bone grafting may be necessary <sup>3</sup>.</p><h4>History and etymology</h4><p>The fibrous cortical defect was first described by <strong>Dallas Burton Phemister </strong>(1882-1951) <sup>5</sup>, an American orthopaedic surgeon in 1929 <sup>6</sup>.</p><h4>Differential diagnosis</h4><p>Possible differential considerations include</p><ul>
- +<li><p><a href="/articles/cortical-desmoid">cortical desmoid</a>: posteromedial aspect of the distal femur</p></li>
- +<li><p><a href="/articles/osteoid-osteoma">osteoid osteoma</a>: night pains</p></li>
- +<li><p><a href="/articles/osteomyelitis">osteomyelitis</a></p></li>
- +<li><p><a href="/articles/stress-fracture">stress fracture</a></p></li>
- +<li><p><a href="/articles/intracortical-osteosarcoma">intracortical osteosarcoma</a></p></li>
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