Two different methods of treatment for open dislocation of the extruded talus without soft tissue attachments (missing talus) were examined. In case 1, a 20-year-old man sustained an open total dislocation of the talus due to a motorcycle accident. The missing talus was found within 3 hr and replaced after thorough washing and debridement. Weightbearing was permitted at 20 weeks; however, the density of the talar body increased in the x-ray and nonweightbearing status was resumed. Reexamination at 2 1/2 years revealed that there was joint space narrowing on the x-ray and decreased pain with ambulation; the patient had returned to his job. In case 2, a 26-year-old man sustained an open total dislocation of the talus with a severe crush wound and impaired circulation to the foot. After thorough washing and debridement of the wound, the calcaneus and distal end of the tibia were aligned. The missing talus was found 3 days later, but not replaced. Weightbearing was allowed on the affected foot at 2 months; however, the patient felt pain at the joint surfaces and arthrodesis was consequently performed. At 2 1/2 years, the patient had a 4.0-cm leg length discrepancy in the involved extremity, but felt no pain when walking. Although reduction of the talus is ideal to preserve function and length of the extremity, several complications can occur. A review of literature on open total dislocation of the talus with extrusion was performed.

Background: Adult human mesenchymal stem/stromal cells (hMSCs) from bone marrow have been reported to exhibit beneficial effects on spinal cord injury (SCI). A neuropeptide, pituitary adenylate cyclase-activating polypeptide (PACAP) is known to decrease neuronal cell death and inflammatory response after ischemia, SCI, and other neuronal disorders. Recently, we found that expression of the gene for mouse PACAP (Adcyap1) was greater in animals receiving hMSCs with neural injury such as ischemia. However, the association of PACAP with hMSCs to protect nerve cells against neural injuries is still unclear.

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Pituitary adenylate cyclase-activating polypeptide (PACAP, encoded by adcyap1) plays an important role in ectodermal development. However, the involvement of PACAP in the development of other germ layers is still unclear. This study assessed the expression of a PACAP-specific receptor (PAC1) gene and protein in mouse bone marrow (BM). Cells strongly expressing PAC1+ were large in size, had oval nuclei, and merged with CD34+ cells, suggesting that the former were hematopoietic progenitor cells (HPCs). Compared with wild-type mice, adcyap1−/− mice exhibited lower multiple potential progenitor cell populations and cell frequency in the S-phase of the cell cycle. Exogenous PACAP38 significantly increased the numbers of colony forming unit-granulocyte/macrophage progenitor cells (CFU-GM) with two peaks in semi-solid culture. PACAP also increased the expression of cyclinD1 and Ki67 mRNAs. These increases were completely and partially inhibited by the PACAP receptor antagonists, PACAP6-38 and VIP6-28, respectively. Little or no adcyap1 was expressed in BM and the number of CFU-GM colonies was similar in adcyap1−/− and wild-type mice. However, PACAP mRNA and protein were expressed in paravertebral sympathetic ganglia, which innervate tibial BM, and in the sympathetic fibers of BM cavity. These results suggested that sympathetic nerve innervation may be responsible for PACAP-regulated hematopoiesis in BM, mainly via PAC1.

The combination in the global ischemia model (i.e., hemorrhagic shock followed by cardiac arrest) caused severe neuronal damage in the central nervous system. Thereby, hind-limb paralysis after global ischemia might result from spinal cord damage. These results suggest that therapeutic strategies for preventing spinal cord injury are necessary when treating patients with severe global ischemia.