Covering of wound infection in hip arthroplasty with local cutaneous flaps.

Total hip arthroplasty is a very common procedure to treat osteoarthritis. One of the complication is the infection which occurs in about 1% of the cases. The manifestation of infection can be poor wound healing with dehiscence and exposition of bone or prosthetic components. Hip arthroplasty infections are difficult to treat. It required an associated multidisciplinary approach with infectiology, orthopedic and plastic surgeries. The study included five patients with hip wound dehiscence after total hip arthroplasty. Coverage after orthopedic surgery was provided by local cutaneous flap. These cutaneous flaps were either a deep inferior epigastric perforator flap (DIEP) or a transposition flap. The orthopedic and the plastic treatment were done at the same time. Two deep inferior epigastric flaps were performed for patients with a deep defect with bone or prosthesis exposure. Four transposition flaps were done in three patients with wound dehiscence but without direct contact with the prosthesis. Three transposition flaps were done from the abdominal wall and one from the posterior thigh. The mean follow up was 18 months, ranging from 10 to 24months. After healing, there was no recurrence of the infection. In all cases, the coverage was obtained. The prosthesis was salvage and the gait was possible. Cutaneous flaps are easy and safe to cover the hip. They are reliable flaps even in patients with multiple co-morbidities. They do not cause sequelae on the recipient site. This study is the first about cutaneous flap for covering hip defects in hip arthroplasty infections.

BRCA1 deficient embryonic stem cells display a decreased homologous recombination frequency and an increased frequency of non-homologous recombination that is corrected by expression of a brca1 transgene.

BRCA1 is a nuclear phosphoprotein that has been classified as a tumor suppressor based on the fact that women carrying a mutated copy of the BRCA1 gene are at increased risk of developing breast and ovarian cancer. The association of BRCA1 with RAD51 has led to the hypothesis that BRCA1 is involved in DNA repair. We describe here the generation and analysis of murine embryonic stem (ES) cell lines in which both copies of the murine homologue of the human BRCA1 gene have been disrupted by gene targeting. We show that exogenous DNA introduced into these BRCA1 deficient cells by electroporation is randomly integrated into the genome at a significantly higher rate than in wild type ES cells. In contrast, integration of exogenous DNA by homologous recombination occurs in BRCA1 deficient cells at a significantly lower rate than in wild type controls. When BRCA1 expression is re-established at 5-10% of normal levels by introduction of a Brca1 transgene into BRCA1 deficient ES cells, the frequency of random integration is reduced to wild type levels, although the frequency of homologous recombination is not significantly improved. These results suggest that BRCA1 plays a role in determining the response of cells to double stranded DNA breaks.