研究尋常性銀屑病（Psoriasis Vulgaris）患者體內基質金屬蛋白酵素（MMP-2）及組織內基質金屬蛋白酵素抑制因子（TIMP-2）與顯微血管密度（MVD）的關係。
方法：在 17 位患者病灶處及 10 位正常人身上取樣作為對照組。基質金屬蛋白酵素
（MMP-2）及基質金屬蛋白酵素抑制因子（TIMP-2）藉由 SP 免疫組織化學染色法。顯微血管密度(MVD)使用CD34單株抗體用免疫組織化學染色法測定。
結果：顯微血管密度在尋常性銀屑病患者身上高於正常人（P<0.01）。基質金屬蛋白酵素及基質金屬蛋白酵素抑制因子在患者的表現中強度，但正常人身上非常低甚至於沒有。基質金屬蛋白酵素與顯微血管密度表現正相關（r = 0.625, P<0.01），基質金屬蛋白酵素抑制因子與顯微血管密度表現負相關（r = -0.424, P<0.01）。
結論：在患者表皮上，基質金屬蛋白酵素可過度表現於細胞與細胞間，細胞與間質間，而患者身上基質金屬蛋白酵素抑制因子的負調控可視為病原因子。患者身上基質金屬蛋白酵素及基質金屬蛋白酵素抑制因子的不正常表現，與顯微血管密度增加極為相關。本研究指出，表淺血管狀態與臨床患者狀況非常相關。總之，患者發病開始局部血管增生時，基質金屬蛋白酵素及基質金屬蛋白酵素抑制因子扮演非常重要的角色。這需要更進一步的研究，或許能解釋患者微血管不正常病理表現基質金屬蛋白酵素及基質金屬蛋白酵素抑制因子。患者皮膚擴大的表皮血管床是維持症狀必須要的，因此這些血管是治療時真實而合理的目標。

Objective: To study the relationship between the expression of matrix
metalloproteinase-2 (MMP-2)、tissue inhibitors of metalloproteinase-2 (TIMP-2) and microvessel density（MVD）in patients with psoriasis vulgaris.
Methods: The biopsies were taken from psoriatic lesions in 17 patients with active psoriasis vulgaris and the skin of 10 normal controls. The expression of MMP-2 and TIMP-2 were detected by the SP
immunohistochemical method. MVD was detected by immunohistochemical method with monoclonal antibody specific for the endothelial marker CD34. Results: MVD in the lesions of psoriasis vulgaris was higher than that in normal control (P<0.01). MMP-2、TIMP-2 were expressed moderate to intense
staining in the psoriatic lesions ，but very weak to absent in the normal skin. The expression level of MMP-2 was positive correlation with MVD(r=0.625，P<0.01),and TIMP-2 was negative associated with MVD in active psoriasis vulgaris(r=-0.424，P<0.01).
Conclusion: The overexpression of MMP-2 could be responsible for cell-cell and cell-matrix changes noted in psoriatic epidermis. Downregulation of TIMP-2 that may serve as an aetiological factor in the development of psoriasis. The abnormal expression of MMP-2 、TIMP-2 protein are closely correlated with the increase of MVD in psoriatic lesions. These findings indicate that there is a close correlation between the state of the superficial vasculature and the clinical status of psoriasis.It was concluded that MMP-2、TIMP-2 might play important roles in the occurrence and progression of angiogenesis in psoriasis. Further mechanistic investigations are required with the potential that MMP-2、TIMP-2 protein may be help to explain the pathogenesis of microvascular abnormalities in
psoriatic skin.The expanded superficial microvascular bed in psoriatic skin is a necessary component for maintaining clinical lesions and these blood vessels are thus a legitimate target for treatment.