Could anyone explain the reasons to supplement A2M to OA knee mainly because there is a lower concentration of A2M in SF than serum (plasma)? Why did the higher A2M in OA's SF (results shown in Fig. 1) not inhibit MMP-13 or other proteases? Perhaps the nature or properties of OA's A2M is/are different than those of normal A2M, and itself may be the problem?

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