Fibrous dysplasia (FD) is a congenital disorder arising from sporadic mutation of the α-subunit of the Gs stimulatory protein. Osseous changes are characterised by the replacement and distortion of normal bone with poorly organised, structurally unsound, fibrous tissue. The disease process may be localised to a single or multiple bones. In McCune-Albright syndrome (MAS), fibrous dysplasia is associated with hyperfunction of endocrine organs and overproduction of melanin in the skin, while Mazabraud syndrome FD is associated with intramuscular myxomas. In radiology, FD is very often automatically associated with the term “ground glass matrix”. However, FD is a complex disease, and knowledge of its unique pathogenesis and course are crucial to understanding imaging findings and potential complications. This article aims to not only summarise the spectrum of radiological findings of osseous and extra-osseous abnormalities associated with FD but also to highlight the pathological base of the disease evolution, corresponding imaging changes and complications based on the disease distribution. We also have provided current recommendations for clinical management and follow-up of patients with FD.Teaching Points• FD is often a part of complex disease, involving not only bone but also multiple other organs.• FD lesions are characterised by age-related histological, radiographical and clinical transformations.• Radiologists play a crucial role in the identification of osseous complications associated with FD.• The craniofacial form of the disease is the most common type of FD and the most difficult form to manage.• Patients with McCune-Albright syndrome may have different extra-skeletal abnormalities, which often require follow-up.

Hürthle cell carcinoma (HCC) has been reported to have variable clinical behavior. The objective of this study was to determine the important prognostic factors in patients with HCC. It was a retrospective investigation of 33 patients with HCC treated in our institution from 1976 to 2002. The average age of our 33 patients with HCC was 55.2 years (range 20-82 years; 23 women, 10 men). Fifteen patients (45.5%) presented with a T2 tumor, 7 (21.2%) with a T3 tumor, and 8 (24.2%) with a T4 tumor; the tumor stage was unknown in three patients. Coexisting papillary carcinoma occurred in six patients (18%), 9% of whom presented with metastatic disease. Twelve patients (36.4%) had metastases, four of whom (12.2%) had persistent HCC, and 8 (24.2%) developed recurrent HCC (range 1-9 years). Eight of these twelve patients (66.7%) died from the HCC. The average follow-up time was 5.5 years (range 1-16 years). Altogether, 3 of 23 women and 5 of 10 men died from their HCC ( p < 0.05). Of the 22 patients with T2-T3 tumors, 5 (22.7%) developed metastases and 1 patient died; 5 of 8 patients (62.5%) with T4 tumors developed metastases and died ( p < 0.01). Patients who were treated by less than total thyroidectomy had a worse prognosis by univariate analysis ( p < 0.01) but not by multivariate analysis. Survival time for patients with persistent disease was shorter than for those with recurrent disease ( p < 0.05). Multivariate analysis, however, revealed no difference for extent of operation or those with persistent and recurrent disease. The cause-specific survivals were 74% and 49% at 5 and 10 years, respectively. Disease-free survivals were 65.0% and 40.5% at 5 and 10 years, respectively. Our findings show that gender and stage of disease influence the prognosis of patients with HCC.

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The subfamily of b2 integrins is implicated in macrophage fusion, a hallmark of chronic inflammation. Among b2 family members, integrin Mac-1 (a M b 2 , CD11b/CD18) is abundantly expressed on monocyte/ macrophages and mediates critical adhesive reactions of these cells. However, the role of Mac-1 in macrophage fusion leading to the formation of multinucleated giant cells remains unclear. Moreover, the role of integrin a D b 2 (CD11d/CD18), a receptor with recognition specificity overlapping that of Mac-1, is unknown. We found that multinucleated giant cells are formed in the inflamed mouse peritoneum during the resolution phase of inflammation, and their numbers were approximately twofold higher in wild-type mice than in Mac-1 À/À mice. Analyses of isolated inflammatory peritoneal macrophages showed that IL-4einduced fusion of Mac-1edeficient cells was strongly reduced compared with wild-type counterparts. The examination of adhesive reactions known to be required for fusion showed that spreading, but not adhesion and migration, was reduced in Mac-1edeficient macrophages. Fusion of a D b 2 -deficient macrophages was also significantly decreased, albeit to a smaller degree. Deficiency of intercellular adhesion molecule 1, a counter-receptor for Mac-1 and a D b 2 , did not alter the fusion rate. The results indicate that both Mac-1 and a D b 2 support macrophage fusion with Mac-1 playing a dominant role and suggest that Mac-1 may mediate cell-cell interactions with a previously unrecognized counter-receptor(s). (Am J Pathol 2016, 186: 2105e2116; http:// dx