Posters— Diagnostic Imaging/Pathology

MYOFIBROBLAST MODULATION IN DESMOID TUMORS

Baldini N, Barbanti-Brodano G, Zini N, Bertoni F, Giunti A (Istituti Ortopedici Rizzoli, 40136 Bologna, Italy)

Myofibroblasts play a role in several conditions, including fibromatoses. During granulation tissue contraction, a high proportion of myofibroblasts develop the expression of a-smooth muscle actin. When contraction stops, myofibroblasts containing a-smooth muscle actin disappear and the scar becomes less cellular and composed of typical fibroblasts. Similarly, during the development of fibrocontractive diseases, fibroblasts acquire contractile features and produce the centripetal force leading to retraction. For this purpose, myofibroblasts develop connections to the surrounding extracellular matrix. The mechanisms leading to the modulation of myofibroblasts remain to be explored. We evaluated a retrospective series of 24 cases of desmoid tumors in order to analyze the expression of a-smooth muscle actin and of CD68 antigen, that identifies reactive mononuclear cells, on paraffin-embedded tissue sections by immunohistochemistry. A positive staining for a-smooth muscle actin, identifying myofibroblasts among the spindle cell component of the lesion, was found in 11/24 cases (46%), whereas the occurrence of CD68-positive mononuclear cells was detected in 19/24 cases (79%). Ultrastructurally, CD68-positive cells were found to correspond to two cell types, i.e. macrophages and mast cells. It may be hypothesized that these elements modulate myofibroblasts through a paracrine mechanism. It is well-known that mast cell proliferation is accompanied by fibrotic changes, possibly through the release of heparin, a molecule that is capable to increase a-smooth muscle actin expression. Moreover, macrophages release growth factors, such as GM-CSF, that are implicated in the modulation of myofibroblasts. It is conceivable that therapeutic agents that interfere with the functional status of spindle cells may be used as a tool for the inhibition of growth of desmoid tumors, as previously demonstrated in other fibrocontractive diseases.