Laparoscopic repair reduces incidence of surgical site infections for all ventral hernias.

BACKGROUND: The role of laparoscopic repair of ventral hernias remains incompletely defined. We hypothesize that laparoscopy, compared to open repair with mesh, decreases surgical site infection (SSI) for all ventral hernia types. METHODS: MEDLINE, EMBASE, and Cochrane databases were reviewed to identify studies evaluating outcomes of laparoscopic versus open repair with mesh of ventral hernias and divided into groups (primary or incisional). Studies with high risk of bias were excluded. Primary outcomes of interest were recurrence and SSI. Fixed effects model was used unless significant heterogeneity, assessed with the Higgins I square (I(2)), was encountered. RESULTS: There were 5 and 15 studies for primary and incisional cohorts. No difference was seen in recurrence between laparoscopic and open repair in the two hernia groups. SSI was more common with open repair in both hernia groups: primary (OR 4.17, 95%CI [2.03-8.55]) and incisional (OR 5.16, 95%CI [2.79-9.57]). CONCLUSIONS: Laparoscopic repair, compared to open repair with mesh, decreases rates of SSI in all types of ventral hernias with no difference in recurrence. These data suggest that laparoscopic approach may be the treatment of choice for all types of ventral hernias.

Review of stoma site and midline incisional hernias after stoma reversal.

BACKGROUND: The incidence of incisional hernias after stoma reversal is not well reported. The aim of this study was to systematically review the literature reporting data on incisional hernias after stoma reversal. We evaluated both the incidence of stoma site and midline incisional hernias. METHODS: A systematic review identified studies published between January 1, 1980, and December 31, 2012, reporting the incidence of incisional hernia after stoma reversal at either the stoma site or at the midline incision (in cases requiring laparotomy). Pediatric studies were excluded. Assessment of risk of bias, detection method, and essential study-specific characteristics (follow-up duration, stoma type, age, body mass index, and so forth) was done. RESULTS: Sixteen studies were included in the analysis; 1613 patients had 1613 stomas formed. Fifteen studies assessed stoma site hernias and five studies assessed midline incisional hernias. The median (range) incidence of stoma site incisional hernias was 8.3% (range 0%-33.9%) and for midline incisional hernias was 44.1% (range 8.7%-58.1%). When evaluating only studies with a low risk of bias, the incidence for stoma site incisional hernias is closer to one in three and for midline incisional hernias is closer to one in two. CONCLUSION: Stoma site and midline incisional hernias are significant clinical complications of stoma reversals. The quality of studies available is poor and heterogeneous. Future prospective randomized controlled trials or observational studies with standardized follow-up and outcome definitions/measurements are needed.

Activation of the extracellular signal-regulated kinases 1 and 2 (ERK1/2) is needed for the TGFß-induced chondrogenic and osteogenic differentiation of mesenchymal stem cells.

The role of the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway on the osteogenesis of progenitor and stem cells has received a lot of attention due to conflicting results in the literature. ERK1/2 has been reported to be both activating and inhibitory to the osteogenesis of different cell types under varying culture conditions. This study focused specifically on the role of ERK1/2 on the chondrogenesis and osteogenesis of mesenchymal stem cells (MSC) induced by cytokine exposure. Bone marrow-derived MSC were cultured in three-dimensional fibrin gel scaffolds and stimulated down the chondrogenic and osteogenic programs by addition of TGF-ß3 to and osteogenic buffer media. Cells were cultured under control conditions (no cytokine supplementation), treated with TGF-ß3 or treated with PD98059+TGF-ß3 for 7 days. RT-PCR results show that addition of TGF-ß3 significantly upregulates the phosphorylation of ERK1/2 and induces the cells down the chondrogenic and osteogenic pathways (as demonstrated by the significant upregulation of aggrecan, sox9, collagen types 1 & 2 gene expressions). Inhibition of ERK1/2 phosphorylation with PD98059 led to the abolishment of the upregulation of chondrogenic and osteogenic-specific gene expressions. These results demonstrate that ERK1/2 is needed for the chondrogenic and osteogenic differentiation of MSC as induced by TGF-ß3 supplementation.