Takagi M, Konttinen Y T, Lindy O, Sorsa T, Kurvinen H, Suda A, Santavirta S
Department of Anatomy, University of Helsinki, Finland.
Clin Orthop Relat Res. 1994 Sep(306):136-44.
Gelatinase/Type IV collagenases, namely, 72 kDa matrix metalloproteinase (MMP)-2 type and 92 kDa MMP-9 type, were analyzed to evaluate the role of extracellular matrix degradation in 17 cases of loosening of total hip endoprostheses. Zymographic and densitometric analyses revealed elevated production of MMP-2 and induction of MMP-9 in tissue extracts from both the interface tissues between bone and implants and the pseudocapsular tissues around the loose endoprostheses when compared with those of 8 control noninflammatory knee synovial tissues. The level of MMP-9 was higher in the interface tissues than in the pseudocapsular tissues. MMP-9 activity was not detected in the control samples. Although differences in the type of prosthetic fixation (cemented versus cementless) or the type of alloy (cobalt-chromium-molybdenum versus titanium-aluminum-vanadium) existed, they shared a similar potential to stimulate tissues to produce MMP-2 and MMP-9. These findings suggest a role for MMP-2 and MMP-9 type gelatinase/Type IV collagenases in the degradation of extracellular matrix of periprosthetic tissues, where they may cause weakening of the connective tissue bed and the loosening of total hip replacement endoprostheses. The pseudocapsular tissues could contribute to the loosening via the production and release of matrix metalloproteinases into the synovial fluid. Alternatively, induction of matrix metalloproteinases in such tissues may reflect remodeling of the pseudocapsular connective tissues.
对明胶酶/IV型胶原酶，即72 kDa基质金属蛋白酶（MMP）-2型和92 kDa MMP-9型进行分析，以评估细胞外基质降解在17例全髋关节假体松动中的作用。酶谱分析和光密度分析显示，与8例对照非炎性膝关节滑膜组织相比，骨与植入物之间的界面组织以及松动假体周围的假包膜组织的组织提取物中MMP-2的产生增加，MMP-9被诱导。界面组织中MMP-9的水平高于假包膜组织。对照样品中未检测到MMP-9活性。尽管假体固定类型（骨水泥型与非骨水泥型）或合金类型（钴铬钼合金与钛铝钒合金）存在差异，但它们刺激组织产生MMP-2和MMP-9的潜力相似。这些发现表明，MMP-2和MMP-9型明胶酶/IV型胶原酶在假体周围组织细胞外基质的降解中起作用，它们可能导致结缔组织床变弱和全髋关节置换假体松动。假包膜组织可能通过产生基质金属蛋白酶并将其释放到滑液中而导致松动。或者，此类组织中基质金属蛋白酶的诱导可能反映了假包膜结缔组织的重塑。
