Multidetector computed tomography (CT) is an excellent way to supplement the radiographic evaluation of problematic hip prostheses. Multidetector CT is well suited for assessing periprosthetic bone, determining precise acetabular cup position, and evaluating periprosthetic fluid collections or ossified masses. Metal implants pose a number of challenges in the performance and interpretation of CT examinations. However, metal artifacts can be minimized by decreasing the detector collimation and pitch, increasing the kilovolt peak and milliampere-seconds, and using appropriate reconstruction algorithms and section thickness. Image interpretation requires a basic understanding of hip reconstruction and hip implants, as well as use of a systematic method of analysis that incorporates prior radiographic findings and CT findings. Radiologists must be familiar with the normal and abnormal CT appearances of hip prostheses and be able to recognize common complications on CT scans.

Imaging is the key to diagnosing and guiding management of bone tumors. Although radiographs are the gold standard for initial imaging evaluation and may make the diagnosis, computed tomography (CT) and magnetic resonance (MR) imaging are important adjunct tools for further characterization as a benign or aggressive lesion, accurately determining matrix composition, assessing lesion extent as well as secondary involvement of nearby structures if malignant, and staging tumors when applicable. In this article, we will highlight important features of CT and MR imaging for bone tumor _________________________________________________________________________________

A 39-year-old man with a history of type 1 diabetes, presented with right hip pain on rotation, of approximately 5 years duration. No significant findings were observed on physical examination. A full blood count and peripheral blood film were unremarkable. Magnetic resonance imaging (MRI) revealed an ovoid, 4 9 3 9 2 cm, hyperintense lesion in the right sacral ala on fluid-sensitive sequences (left). The lesion was confined to the bone on MRI, and there was no apparent cortical destruction on MRI or a subsequent computerized tomography (CT) scan. A CT-guided core biopsy demonstrated sheets of small to intermediate atypical lymphoid cells with irregular nuclei, indistinct nucleoli, distinct cell borders and ample cytoplasm varying from clear to granular (right). Only rare mitotic and apoptotic figures were seen. These atypical cells were positive for CD20, PAX5, BCL2, TRAP, CD72 (DBA44), CD25, CCND1 and kappa light chain, and negative for CD10, CD5, CD117, CD138, CD56, CD43, myeloperoxidase and lambda light chain. No evidence of CCND1/IGH fusion was detected by FISH, essentially ruling out the possibility of mantle cell lymphoma. A BRAF V600E mutation was detected by polymerase chain reaction. Based on the overall morphological, immunophenotypic and molecular features, a diagnosis of hairy cell leukaemia was made. A subsequent staging bone marrow biopsy was performed and showed no evidence of involvement by a lymphoproliferative disorder. The spleen was not visualized on imaging of the pelvis but was not palpable. Treatment was initiated in the form of systemic chemotherapy and the patient commenced a 7-d course of continuous cladribine 0Á1 mg daily without adverse effects. He achieved and maintained radiographic remission throughout a 6-month followup period.Very rarely, hairy cell leukaemia presents as an isolated mass (lymphomatous form) without apparent bone marrow, blood or spleen involvement. This unusual form of hairy cell leukaemia expresses the distinctive immunohistochemical and genetic hallmarks of classical hairy cell leukaemia, and is a plausible consideration in the differential diagnosis of B-cell neoplasms presenting as a mass. The effectiveness of cladribine therapy in these cases suggests that this variant is comparable to hairy cell leukaemia presenting classically.

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