Repair after a localized injury is prolonged in the masseter as compared to the limb muscle tibialis anterior (TA). However, it has yet to be established if this defect in repair resides in satellite cell number, in their ability to effectively activate and proliferate in response to factors released in injury or in inflammatory response mechanisms. Objective: Examine events in the inflammatory response to a freeze-induced injury in masseter and TA. Methods: To identify and quantify different populations of inflammatory cells within masseter and TA after damage, freeze-injured posterior superficial masseter and TA were harvested from 5-females at 1 (T1), 4 (T4), 7 (T7), 14 (T14) and 21 (T21) days post injury, and from 4 female controls. Consecutive 14µm cryosections were immunostained to detect specific inflammatory cell markers. Cells/area immunopositive for each marker were determined in a series of 3-sections, 500mm apart using Image Pro Plus software. In adjacent Toluidine blue collages, the extent of damage and repair was assessed. Data were evaluated using Kruskal-Wallis ANOVA. Results: In both masseter and TA, the damaged region was characterized by massive necrosis and inflammatory cell infiltration at T1. In both muscles at T4, small fibers had formed at the margin of the damaged region; by T7 this entire region was filled with small fibers. However, in masseter, inflammatory cells could be detected within the repaired region at T14 and T21, associated with regions of necrosis, whereas in TA normal muscle architecture was restored. Whereas macrophage cell numbers in damaged regions in did not differ significantly between masseter and TA during the first week of repair, mast cell numbers were significantly increased in masseter at both early and later time-points (p<0.05). Conclusion: Prolonged repair in masseter muscle may be a consequence of its inflammatory response to damage.