NONOSSIFYING FIBROMA OF LONG BONES - AN IMMUNOHISTOCHEMICAL STUDY

Fourteen cases of nonossifying fibroma (NOF) of bone were studied immu nohistochemically to elucidate the character of their constituent stro mal cells, multinucleated osteoclastic-type giant cells, and foam cell s. The stromal spindle cells, the main cellular component of NOF, stai ned for KP-1 (CD-68), alpha-1-antichymotrypsin, and HAM-56 in all case s and were immunoreactive for alpha-1-antitrypsin and HLA-DR in 13 (93 %) cases and for lysozyme in 8 cases (57%). These results indicate tha t the cells have a histiocytic immunophenotype. However, they also exp ressed vimentin and muscle-specific actin (MSA) in 14 (100%) and 13 (9 3%) cases, respectively, indicating that they might also have fibrobla stic or myo-fibroblastic characteristics. This histiocytic-mesenchymal immunophenotype was present in most of the stromal cells; from 50 to 100% of them coexpressed KP-1, vimentin, and MSA. The stromal cells we re essentially the only cells reactive for proliferating cell nuclear antigen (PCNA) and Ki-67 antigen, which were present in the cells of 1 3 (93%) and 10 (77%) of the cases, respectively. The multinucleated gi ant cells and foam cells also showed immunohistochemical evidence of h istiocytic differentiation. The former were reactive for KP-1 in all 1 4 cases, for lysozyme in 13 (93%), and for alpha-1-antichymotrypsin in 8 of 13 cases (62%). Foam cells expressed reactivity for KP-1, lysozy me, HLA-DR, and HAM-56 in all of the cases in which they were present, whereas leukocyte common antigen (LCA) expression was present in 66% of the cases. The findings in our study indicate that the stromal cell s in nonossifying fibroma are the proliferative elements and that they possess immunohistochemical features of both histiocytic and fibrobla stic-myofibroblastic differentiation. The foam and multinucleated gian t cells appear to represent an end stage of cellular development lacki ng proliferative properties; their origins appear linked to that of th e stromal cells. There was no support for the suggestion that NOF is a lipoblastic lesion, as all cells were nonreactive for S-100 protein.