It has been reported that following nerve injury, MMP-9 is transiently upregulated in injured DRG and participates in neuropathic pain induction, whereas MMP-2 displays a delayed increase in DRG and DHSC and is involved in a later phase of neuropathic pain maintenance [10]. So far, no characterization of MMPs expression in the CFA model of inflammatory pain has been carried out. Thus, we first examined MMP-2 and MMP-9 expression patterns in the DRG and DHSC during CFA-induced inflammatory pain. As shown in Figure  8A and 8B, MMP-9 mRNA levels were transiently upregulated in DRG on days 15 (×3.95 ± 0.55, **P < 0.01, n = 4) and 21 (×2 ± 0.36, *P < 0.05, n = 4) as well as in the DHSC 15 days (×2.8 ± 0.6, *P < 0.05, n = 4) after CFA injection, and returned to levels of sham rats thereafter. Markedly, MMP-2 expression showed no variation in DRG, but a mean 2-fold persistent upregulation in DHSC at late stages (×3.45 ± 0.66 on day 15; ×2 ± 0.66 on day 21 and × 1.94 ± 0.36 on day 60 post-CFA, *P < 0.05, n = 4). Moreover, dexamethasone treatment at late stages of inflammatory pain repressed MMP-2/-9 expression in DRG and DHSC of CFA rats ( Figure 8C and 8D, *P < 0.05, **P < 0.01, n = 4). Thus, the induction of MMP-2 and MMP-9 mirrors reduced NOV expression at late stages in the establishment of inflammatory pain ( Figure 3A and 3B). In an acute model of inflammatory pain, carrageenaninduced mechanical allodynia is partially prevented in MMP-9-null mice [ [10], suppl. data]. To test whether MMP-9 could impact CFA-induced persistent inflammatory pain, the mechanical allodynia of CFA rats treated with an MMP-9 inhibitor (MMP-9i) was evaluated using the von Frey filament test. As shown in Figure 8E, repeated intrathecal injections of MMP-9 inhibitor from day 9 to day 12 post-CFA injection significantly attenuated mechanical allodynia (5.5 ± 0.8 g in CFA rats treated with MMP-9i compared to 2.7 ± 0.3 g in CFA rats injected with vehicle, **P < 0.01, n = 6). Altogether, these **data** suggest a role for MMP-9 in the maintenance of CFA-induced inflammatory pain.