Objectives-To report the clinical utility of high-resolution ultrasound (US) for monitoring vascular compromise after free tissue transfer.Methods-Fifty-two tissue transfers in the extremities were included in this study. Blood flow around the anastomotic pedicle and subcutaneous tissue of the grafted flap was monitored with pulsed color and power Doppler US whenever the conventional monitoring method, comprising the bedside assessment of the temperature, capillary refill, and flap color, showed abnormalities until 1 week after reconstruction.Results-All flaps were indicated for US monitoring, with 44 flaps showing Doppler signals in each position, even though conventional flap monitoring showed an abnormality. Forty of the 44 flaps showed no flap failure, whereas the remaining 4 flaps developed partial necrosis. Abnormal US findings were noted in 8 of the 52 flaps. Ultrasound revealed interruption of venous blood flow around the anastomotic pedicle in 6 of 8 flaps. Emergent exploration revealed venous occlusion at the anastomotic pedicle, similar to the US finding. In 2 of the 8 flaps, US showed no blood flow to either the anastomotic pedicle or subcutaneous tissue. Emergent exploration revealed arterial occlusion at the anastomotic pedicle. Seven of the 8 reexplored flaps were salvaged after revision surgery with complete flap survival. Partial flap survival was noted in 1 case, but complete flap failure was avoided.Conclusions-Ultrasound is a useful adjunct that enables a direct assessment of perfusion in grafted tissues, which may reduce unnecessary exploration when conventional flap monitoring shows an abnormality.
The role of substance P on maintaining ligament homeostasis by inhibiting endochondral ossification during osteoarthritis progression
AimOsteoarthritis (OA) is a disease in which degeneration occurs in various tissues such as cartilage and subchondral bone. Degeneration of ligaments also plays an important role in OA progression, resulting in an increase in chondrocytes and ossification, but the factor that causes this is still unclear. It is reported that the expression of calcitonin gene‐related peptide (CGRP) increases OA progression, and CGRP might play a role in ligament degeneration because CGRP has a function in endochondral ossification. The purpose of this study is to analyze the mechanism of ligament degeneration and the function of CGRP.MethodsTo examine the relationship between ligament degeneration and CGRP expression, human posterior cruciate ligaments (PCL) from OA patients, and senescence‐accelerated mouse prone 8 (SAMP8) mice were histologically analyzed. The effect of CGRP on human ligament cells on chondrogenesis, osteogenesis, and adipogenesis was also examined.ResultsIn human PCL and SAMP8 mice, CGRP expression increased as degeneration progressed, and decreased in severe degeneration. CGRP was expressed in the chondrocyte‐like cells with SOX9. CGRP‐positive cells expressing type II collagen increased with OA progression. CGRP upregulated the gene expression of VEGF, SOX9, RUNX2, COL10a1, and MMP13 in the human ligament cells. CGRP also promoted chondrogenesis and osteogenesis from the human ligament cells.ConclusionDuring OA progression, CGRP plays a role in the transdifferentiation from ligament cells to chondrocytes and promotes endochondral ossification in the ligament. CGRP would be the therapeutic target to prevent ligament degeneration.
Background Degeneration occurs in various tissues such as cartilage and subchondral bone, and ligament deficiency also plays an important role in the osteoarthritis (OA) progression, but factor which it causes is still unclear. Calcitonin gene-related peptide (CGRP), one of the neuropeptides, its expression increases in OA progression. The purpose of this study is to analyze the mechanism of ligament degeneration and the function of CGRP. Methods To examine the relationship between ligament degeneration and CGRP expression, human posterior cruciate ligament (PCL) from OA patients and SAMP8 mice were histologically analyzed. The effect of CGRP of human ligament cells on the differentiation was also examined. Results In human PCL, CGRP expression increased as degeneration progressed, and decreased in the severe degeneration. CGRP expressed in the chondrocyte like cells with SOX9. In SAMP8 mice, the expression of CGRP increased as OA progression, but it decreased in the severe OA. CGRP up regulated the gene expression of VEGF, SOX9, RUNX2, Col10a1and MMP13. CGRP also promoted chondrogenesis and osteogenesis in the human ligament cells. Conclusions During OA progression, CGRP induces the transdifferentiation from ligament cells to chondrocytes, and promotes endochondral ossification in the ligament. CGRP would be the therapeutic target to prevent the ligament degeneration.
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