Donor site morbidity and quality of life after microvascular head and neck reconstruction with free fibula and deep-circumflex iliac artery flaps.

PURPOSE: Bone defects after resective tumor surgeries often require the use of microvascular reanastomized bone grafts for reconstruction. The decision as to which specific flap is most suitable for the particular patient is dependent on various factors. The aspects donor site morbidity and quality of life are rarely taken into account in this connection. The aim of this study was to analyze whether these factors, in the future, should influence the choice of donor site. MATERIAL AND METHODS: In this study, the donor sites of 46 patients with respect to deep-circumflex iliac artery (DCIA) and fibula flaps were analyzed using subjective and objective parameters. The primary outcome was postoperative pain measured by VAS. Postoperative complication evaluations as well as 2 orthopedic scores were implemented (American Orthopedic Foot and Ankle Society (AOFAS) Ankle-Hindfoot Score and Harris Hip Score) and the patients' quality of life was assessed using the 36-Item Short Form (SF-36) questionnaire to quantify donor site impairment. RESULTS: Postoperative pain was rated with a mean value of 42.4 mm (SD 34.8) for the DCIA group and 36.9 mm (SD 37.1) for the fibula group (p = 0.617). After a mean period of 13.72 months, pain was rated with a mean value of 15.3 mm (SD 21.7) for DCIA and 13.3 mm (SD 22.6 mm) for the fibula (p = 0.763). Persistent pain, however, was recorded only in 11.11% of DCIA patients and 5.26% of fibula patients. Furthermore pain intensity was higher in the DCIA group. A changed gait pattern was observed in 59.26% of DCIA patients and 21.05% of fibula patients. DCIA patients required walking aids for walking and stair climbing more often. Looking at the results of the 2 orthopedic scores, fibula patients showed slightly better results. Concerning quality of life, patients after reconstructive surgery with DCIA flaps showed slight better results than patients in the fibula group. CONCLUSIONS: Taking the results of this study into account, the outcome in terms of pain, morbidity and quality of life did not show a significant superiority of any donor site.

Effect of the abrogation of TGF-beta1 by antisense oligonucleotides on the expression of TGF-beta-isoforms and their receptors I and II in isolated fibroblasts from keloid scars.

Disequilibrium of dermal wound repair can result in continued accumulation of ECM and excessive scar formation. In susceptible genetically predisposed individuals, keloid formation can be observed. Keloid disease represents a benign dermal fibroproliferative tumor that is unique to humans. TGF-beta is known to play a key role in the pathogenesis of this disease which is still not fully understood. The isoforms TGF-beta1 and TGF-beta2 have profibrotic properties, whereas TGF-beta3 may have antifibrotic functions. TGF-beta exerts its influence by binding to type I and type II TGF-beta receptors, thereby forming a complex and activating specific downstream effector molecules. The aim of this study was to investigate the effect of TGF-beta1 targeting by antisense oligonucleotides on the RNA synthesis and protein expression of TGF-beta isoforms and their receptors in keloid-derived fibroblasts. In tissue samples with normal fibroblasts (NFs) serving as control samples, expression of TGF-beta1 and -beta2 was decreased when compared to keloid fibroblasts (KFs), while expression of TGF-beta3 and of TGF-betaRII was significantly higher in NFs. In the ELISA assay, abrogation of TGF-beta1 led to a significant decrease in TGF-beta1 and -beta2 (p<0.05). Expression of TGF-beta2 mRNA was reduced. Expression of TGF-beta3 mRNA revealed contrary patterns in KFs from different patients while expression of TGF-betaRI was found to be equal during the measurement period. TGF-betaRII mRNA expression was increased after 48 and 72 h respectively. There is growing evidence for a regulatory mechanism between TGF-beta1 and its receptors. Our findings support this theory by suggesting interrelations between the different TGF-beta isoforms and their receptors. Abnormal response of KFs to TGF-betamight reflect a modification in the regulatory pathway that occurs at the receptor level or during intracellular trans-duction. Improving the understanding of TGF-beta in keloid disease could lead to the development of clinically useful therapeutic modalities for treatment of keloid disease or even allow identification of preventive strategies.