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.
They are asymptomatic and self-limiting, completely healing by adulthood.
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 2.
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 2-3.
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
- no periosteal reaction
Signal characteristics include:
- T1: hypointense
- T2: variable, depending on the phase of healing 3
Nuclear medicine (bone scan)
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 even follow-up is required in typical cases. If associated with pathological fracture (more common in NOF) 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
It was first described by Dallas Burton Phemister (1882-1951) 5, the American orthopaedic surgeon in 1929 4.
Possible differential considerations include
- 1. Bullough PG, Walley J. Fibrous cortical defect and non-ossifying fibroma. Postgrad Med J. 1965;41 (481): 672-6. doi:10.1136/pgmj.41.481.672 - Free text at pubmed - Pubmed citation
- 2. Goodin GS, Shulkin BL, Kaufman RA et-al. PET/CT characterization of fibroosseous defects in children: 18F-FDG uptake can mimic metastatic disease. AJR Am J Roentgenol. 2006;187 (4): 1124-8. doi:10.2214/AJR.06.0171 - Pubmed citation
- 3. Betsy M, Kupersmith LM, Springfield DS. Metaphyseal fibrous defects. J Am Acad Orthop Surg. 12 (2): 89-95. J Am Acad Orthop Surg (full text) - Pubmed citation
- 4. Phemister DB. CHRONIC FIBROUS OSTEOMYELITIS. (1929) Annals of surgery. 90 (4): 756-64. Pubmed
- 5. GILCHRIST RK. Dallas Burton Phemister 1882-1951. (1952) Transactions of the ... Meeting of the American Surgical Association. American Surgical Association. Meeting. 70: 431-2. Pubmed