Temporal profile of microvascular disturbances in rat tibial periosteum following closed soft tissue trauma.

BACKGROUND AND AIMS: Bone devascularization due to impaired periosteal perfusion following fracture with severe soft tissue trauma has been proposed to precede and underlie perturbed bone healing. The extent and temporal relationship of periosteal microcirculatory deteriorations after severe closed soft tissue injury (CSTI) are not known. We hypothesized that periosteal microcirculation is adversely affected and the manifestation of trauma-initiated microvascular impairment in periosteum is substantially prolonged following CSTI.
MATERIAL AND METHODS: Using the controlled-impact injury device, we induced standardized CSTI in the tibial compartment of 35 isoflurane-anesthetized rats. Following the trauma the rats were assigned to five groups, differing in time of analysis (2 h, 24 h, 48 h, 1 and 6 weeks). Non-injured rats served as controls. Before the metaphyseal/diaphyseal periosteum was surgically exposed, intramuscular pressure within tibial compartment was measured. Using intravital fluorescence microscopy (IVM) we studied the microcirculation of the tibial periosteum. We calculated the edema index (EI) by measuring the skeletal muscle wet-to-dry weight ratio (EI = injured limb/contralateral limb).
RESULTS: Microvascular deteriorations of periosteal microhemodynamics caused by isolated CSTI were reflected by persistent decrease in nutritive perfusion, markedly prolonged increase in microvascular permeability associated with increasingly sustained leukocyte rolling and adherence throughout the entire study period, mostly pronounced 48 h after the trauma. Peak level in capillary leakage coincided with the maximum leukocyte adherence, tissue pressure, and edema. Microcirculation of tibial periosteum in control rats demonstrated a homogeneous perfusion with no capillary or endothelial dysfunction.
CONCLUSION: Isolated CSTI in absence of a fracture exerts long-lasting disturbances in periosteal microcirculation, suggesting a delayed temporal profile in manifestation of CSTI-induced periosteal microvascular dysfunction and inflammation. These observations may have therapeutic implications in terms of preserving periosteal integrity and considering the interaction of skeletal muscle damage and periosteal microvascular injury during management of musculoskeletal trauma.