Fibrous Cortical Defect

Updated: Dec 15, 2017
  • Author: Bernardo Vargas, MD; Chief Editor: Harris Gellman, MD  more...
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Overview

Background

Fibrous cortical defect (FCD; also referred to as nonossifying fibroma [NOF] or nonosteogenic fibroma) was first described by Phemister in 1929. Sontag and Pyle reported a radiologic description in 1941, [1] and in 1942, Jaffe and Lichtenstein described clinical and anatomic aspects and the natural history. [2]

FCD probably is the most frequent bony lesion in children, occurring in as many as 30-40%. [3] It is most common in adolescents. The term FCD was coined to describe the smaller variety of NOF [4] ​; for a lesion large enough to encroach on the medullary canal, the term NOF is used. However, no histologic difference exists between these lesions. The authors believe that FCD and NOF should be considered the same entity, and in this article, the two terms are interchangeable. These lesions are, in fact, developmental abnormalities, as opposed to benign neoplasms.

FCD usually is an incidental finding on radiographs. Always benign, it may result in pathologic fracture, though this is is a rare first presentation. [5] These lesions can exist in multiple sites. FCD may be difficult to diagnose in the presence of pain or swelling of soft tissues. It also can be confused with a more aggressive lesion [6, 7] ; therefore, biopsy may be necessary. Fractures and impending fractures are indications for surgical intervention. Association with other bone lesions, such as aneurysmal bone cyst, is rare. [2, 4, 8, 9, 10, 11]

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Pathophysiology

The average duration of FCD is in the range of 29-52 months, after which period the lesion spontaneously resolves. FCD may be present during childhood, but lesions tend to disappear in adolescence.

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Etiology

The etiology of FCD remains obscure. FCD is a proliferation of benign fibrous tissue, possibly developing as a result of periosteal injury or secondary to abnormalities at the epiphyseal plate. Others postulate that FCD is related to the normal cutback phenomenon seen in maturing physeal plates. Progression of this lesion introduces abnormal tissue into the metaphyseal cortex.

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Epidemiology

FCD constitutes 5% of benign tumoral lesions of bone. The true incidence is more likely to be on the order of 30% or more, but because FCD is asymptomatic in most patients, most lesions are never identified. Sontag and Pyle identified this lesion in 54% of boys and 22% of girls in a series of 200 healthy children. [3, 12] These lesions occur in multiple sites in approximately 50% of patients. FCD is rare in children younger than 2 years and is most common in adolescents.

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Prognosis

The rarity of FCDs in adults confirms that these lesions regress with time. The prognosis is excellent in those unusual cases where patients require curettage and bone graft. [13]

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