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In order to elucidate the causes of ossification in spinal ligaments, ultrastructural alteration and immunolocalization of transforming growth factor-beta (TGF-beta), as well as that of the TGF-beta receptor were examined during the chondrification of ligamentous fibroblasts, by inducing ossification in ligamenta flava of murine lumbar spines, employing recombinant human bone morphogenetic protein-2 (rhBMP-2). Normal ligamenta flava, consisting of flattened fibroblasts, showed no immunolocalization of TGF-B isoforms. From the second week following BMP-administration, cartilage gradually replaced the ligaments. Cells in the central portion of the ligament contained abundant Golgi apparatus as well as enlarged endoplasmic reticula. Proliferative or hypertrophic chondrocytes in this area showed immunoreactivity to TGF-beta(3) latency-associated peptide, while calcified hypertrophic chondrocytes accompanied by both matrix vesicle-and collagen-calcification were noticed at the insertion site to spinal lamina, where there was no immunolocalization of this peptide. In addition, the TGF-beta type I receptor was localized on the proliferative and hypertrophic cells of the central portion. Therefore, as regards the pathological chondrification of ligamentous fibroblasts induced by exogenous BMP-2, TGF-beta is speculated to promote matrix-formation and chondrocytic maturation, under the autocrine/paracrine system, in concert with exogenous BMF-2.

acta histochemica et cytochemica

Ultrastructure and Immunolocalization of Transforming Growth Factor-Beta in Chondrification of Murine Ligamentous Fibroblasts and Endochondral Calcification Induced by Recombinant Human Bone Morphogenetic Protein-2.