DIFFERENTIATION AND PROLIFERATIVE ACTIVITY IN BENIGN AND MALIGNANT CARTILAGE TUMORS OF BONE

To assess the histological grade in benign and malignant cartilage tum ors of bone by more objective methods, we examined the differentiation and proliferative activity of tumor cells in six enchondromas, five c hondroblastomas, and 13 chondrosarcomas immunohistochemically. A varia ble number of cells in all tumors showed S-100 protein and vimentin im munoreactivity. In fully differentiated cartilage of enchondromas and low grade chondrosarcomas, tenascin, which is an extracellular matrix glycoprotein, was present in small amounts or absent but was increased at the periphery of tumor lobules and even in the matrix throughout t he high grade chondrosarcomas. Higher rate and intensity of proliferat ing cell nuclear antigen (PCNA) reactivity were found in chondrosarcom as, especially in spindle-shaped cells of high grade tumors, than in e nchondromas. The distribution of PCNA-positive cells almost correspond ed to the regions with tenascin reactivity. One tumor of high grade ch ondrosarcoma showed p53 protein immunoreactivity. Aberrant expression of cytokeratin was observed in four chondroblastomas. The expression o f desmin was identified in relatively large proportions of enchondroma s and chondrosarcomas, regardless of their benign or malignant nature and histological grade. Smooth muscle or muscle-specific actins also w ere present in a smaller number of tumors. Based on these findings, it is concluded that unusual staining characteristics were present, in a ddition to those of a chondroblastic nature, in the cartilage tumors o f bone. Tenascin and PCNA positivity of various degrees in all chondro blastomas may suggest that they are chondrogenic tumors having a relat ively high proliferative activity, albeit their benign clinical course . Proliferative activity of tumor cells in enchondromas and chondrosar comas correlated well with their histological grade. Tenascin may play a role in promoting tumor cell proliferation of cartilagenous neoplas ms and, on the other hand, the alterations of extracellular matrix inv olving tenascin synthesis seem to be a result of tumor development. Hu nt PATHOL 26:838-845. Copyright (C) 1995 by W.B. Saunders Company.