Free omental tissue transfer is a versatile reconstructive option for trunk, head and neck, and extremity reconstruction. Its utility is due to the length and caliber of the vascular pedicle and the malleability and surface area of the flap. We report our experience with omental free flap coverage of complex upper-extremity defects.

Adequate coverage of complex, composite scalp defects in previously radiated, infected, or otherwise compromised tissue represents a challenge in reconstructive surgery. To provide wound closure with bony protection to the brain, improve cranial contour, and prevent or seal cerebrospinal fluid (CSF) leaks, composite free tissue transfer is a reliable and safe option. We report our experience with the latissimus dorsi/rib intercostal perforator myo-osseocutaneous free flap in the reconstruction of bony and soft tissue defects of the cranium and overlying scalp. The surgical technique, design, and outcomes of the latissimus dorsi/rib intercostal perforator myo-osseocutaneous free flap reconstruction in five patients with cranial defects between 2003 and 2007 were retrospectively evaluated. Patient characteristics, defect size, underlying cause, reconstructive details, and complications were analyzed. All patients (age 43 to 81) had composite defects ranging from 36 to 750 cm2 (mean size 230 cm2) for the bony component and from 16 to 400 cm2 (mean size 170 cm2) for the soft tissue defect. All patients had a history of prior or current infection of the affected area, and two patients had a CSF leak. Defects were due to malignancy and infection (n = 2), infiltrative cutaneous mucormycosis with osteomyelitis (n = 1), and hemorrhagic stroke requiring craniectomy (n = 2), complicated by infection and failed cranioplasty in one patient and continuous CSF leak in the other. The latissimus dorsi composite free flap consisting of skin, muscle, and vascularized rib can successfully cover large complex cranial defects, provide skeletal support, improve contour, and significantly enhance functional outcome with limited donor site morbidity.

Background Bone morphogenetic proteins (BMPs) play a sentinel role in osteoblastic differentiation, and their implementation into clinical practice can revolutionize cranial reconstruction. Preliminary data suggest a therapeutic role of adenoviral gene delivery of BMPs in murine calvarial defect healing. Poor transgene expression inherent in direct adenoviral therapy prompted investigation of cell-based strategies. Objective To isolate and immortalize calvarial cells as a potential progenitor source for osseous tissue engineering. Materials & Methods Cells were isolated from murine skulls, cultured, and transduced with a retroviral vector bearing the loxP-flanked SV40 large T antigen. Immortalized calvarial cells (iCALs) were evaluated via light microscopy, immunohistochemistry, and flow cytometry to determine whether the immortalization process altered cell morphology or progenitor cell profile. iCALs were then infected with adenoviral vectors encoding BMP-2 or GFP and assessed for early and late stages of osteogenic differentiation. Results Immortalization of calvarial cells did not alter cell morphology as demonstrated by phase contrast microscopy. Mesenchymal progenitor cell markers CD166, CD73, CD44, and CD105 were detected at varying levels in both primary cells and iCALs. Significant elevations in alkaline phosphatase activity, osteocalcin mRNA transcription, and matrix mineralization were detected in BMP-2 treated iCALs compared to GFP treated cells. Gross and histological analyses revealed ectopic bone production from treated cells compared to controls in an in vivo stem cell implantation assay. Conclusion We have established an immortalized osteoprogenitor cell line from juvenile calvarial cells that retain a progenitor cell phenotype and can successfully undergo osteogenic differentiation upon BMP-2 stimulation. These cells provide a valuable platform to investigate the molecular mechanisms underlying intramembranous bone formation and to screen for factors/small molecules that can facilitate the healing of osseous defects in the craniofacial skeleton.

Cortical spreading depression (CSD) is accompanied by hyperemia followed by long-lasting hypoperfusion and impaired cerebrovascular reactivity. The authors show that vasodilation to extraluminal acidosis (pH 7.0) and increased concentrations of extraluminal potassium (12, 20, 40 mmol/L) was significantly reduced in isolated rat middle cerebral arteries after CSD in vivo before the artery was isolated, compared with sham-operated controls. Application of 80-mmol/L potassium induced vasoconstriction after CSD. Therefore, the impairment of vascular reactivity after CSD in vivo occurs, at least in part, at the vascular level itself.

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