The Preliminary Study Of The Pathogenesis Of Cavernous Venous Malformation Of Body Surface

Objective To probe the pathogenesis of CVM of body surface on the basis of itspathologic structure.(1) Observe the pathologic structure of CVM and study thedistribution and phenotype of EC and SMC in it.(3) Investigate the expression of thestructure protein and vascular groW-th factor in malfOrmation to probe the pathogenesisof the abnormal sinusoid wall in it.(4) Investigate the nerve distribution in CVM and thetissue around it to understand the relation between the nerve distribution andmalformation.Method 42 specimens of CVM,l2 specimens of medium-sized vein and l2specimens of small vein are included in our study.(1) H-E stain was used to observe thepathologic structure of CVM,particulary the distribution of EC and SMC and calculatethe number of EC and SMC in the vessel wall of malformation and small veins.(2) 25specimens of CVM and all specimens of medium-sized and small veins are selected forimmunohistochemistry stain with EnVision method.@ The monoclonal antibody antiCD31 and Q -SMA which are the markers of EC and SMC are used for observing thephenotype of these two kinds of cell.@ The monoclonal anibody anti N-Co1lagen,Fibronectin and Laminin are used for investigating the expression of structure protein.@ The monoclonal antibody ani VEGF, TGF-6, and Ang-1 are used for investigatingthe expression of vascular groWth factor.@ The monoclonal antibody anti NSE and NFare used for investigating the nerve distribution.Result (l) The ratio of radius and thickness of cavemous venous mafformations ishigher obviously than moderate and small veins. The sinusoid wall does not increas itsthickness consistent with the expanding of lumen of sinusoid. (2) The ratio of ECs toSMCs in malfOrmations is less obviously than in small veins, The expression of Q -SMA in malformations is less obviously than in medium-sized and small veins,and theorganization is more confused;The expression of CD31 in them is similar.(3) Theexpression of IV-Collagen, Fibronectin and Laxninin in CVM is less obviously than inmedium-sized and small veins,but the distribution is similar.(4) CVM and small veinsexpressed VEGF stronger than medium-sizes veins .There is no difference in theexpression of TGF- 0,.The small veins express Ang-l strongest.(5) There is hardly nonerve distribution in CVM.-- 3 --$=vkX%@tcF{4itx #x J%@Conclusion (1) The EC and SMC in sinusoid wall of maIfOrmation developdisproportionally and the SMCs have an abnormal phenotype,Which is the majorpathologic basis of CVM. (2) The low expression of IV-Collagen, Fibronectin andLaminin playes important role in the pathogenesis of the abnorma1 sinusoid wall inCVM.(4) There is disturbance of vascular remodelling in the development of sinusoidwal1 in CVM,which may be caused by the defect of Ang-l-Tie-2 signal transductionpathway. (5) The defect of nerve distribution in CVM have close relationship with theoccurrence and progress of CVM.