The effects of unrestricted motion on the surfaces of injured, healing tissue are largely speculative. To study this phenomenon, a new model employing 54 primate tendons and stereomorphometric image analysis was used to quantitate adhesion volume after a standardized surface injury. Three randomized groups (n = 18 per group) were studied: group I, incision/resection; group II, incision/resection plus ischemia; and group III, ischemia alone. The moving surfaces were observed at intervals from 1 week to 2 1/2 years using dissecting, light, and scanning electron microscopy. Fibroblasts were found to invade the traumatized segment from sources both intrinsic and extrinsic to the tendon, generating adhesive bands whose volume correlated with the degree of initial injury. The defect was ultimately effaced by scar, yet the continuous motion appeared to modify the healing by lengthening adhesive elements and by establishing a smooth, functional "neosheath" that coalesced from the overlying soft tissues. This proliferative response occurred in all specimens, peaked during the third week, and limited normal motion in only 12 percent. This model, the first to successfully study such surfaces in primates, also indicates that closure of the tendon sheath is unnecessary.