Profit Analysis of Minimal-invasive Approaches for Surgical Treatment of A3 Spinal Burst Fractures.

BACKGROUND/AIM: Regarding the surgical treatment of incomplete burst fractures of the spine, no optimal standard procedure has been established. While previous studies have focused on radiological and surgical outcome parameters, the literature has not elucidated economic aspects of various surgical treatment options in detail yet. This study aimed to investigate whether open and minimal-invasive approaches differ in their economic profit gain. Furthermore, we examined whether a single-stage or two-stage approach of anterior-posterior fusion was more profitable. PATIENTS AND METHODS: By analyzing retrospectively data of 129 patients who underwent surgical procedure due to isolated incomplete burst fractures, we examined the economic profit and radiological parameter of open pedicle screw insertion, minimal-invasive techniques (percutaneous screws, percutaneous screws combined with SpineJack®, kyphoplasty or SpineJack®), and anterior-posterior fusion. RESULTS: Percutaneous screws in combination with SpineJack® gained significantly higher profit and higher profit per day of hospital length of stay. Profit was similar after single-stage and two-stage approach of vertebral body replacement. No significant difference in radiological outcome after 24 months was detected between the various surgical techniques. CONCLUSION: From a financial aspect, our finding suggests that application of percutaneous screws in combination with SpineJack® may generate the highest economic profit gain regarding treatment of incomplete burst fracture.

Gut Microbiota-Derived Propionate Regulates the Expression of Reg3 Mucosal Lectins and Ameliorates Experimental Colitis in Mice.

BACKGROUND AND AIMS: Regenerating islet-derived protein type 3 [Reg3] lectins are antimicrobial peptides at mucosal surfaces of the gut, whose expression is regulated by pathogenic gut microbes via interleukin-22- or Toll-like receptor signalling. In addition to antimicrobial effects, tissue protection is hypothesized, but has been poorly investigated in the gut. METHODS: We applied antibiotic-induced microbiota perturbations, gnotobiotic approaches and a dextran-sodium sulfate [DSS] colitis model to assess microbial Reg3 regulation in the intestines and its role in colitis. We also used an intestinal organoid model to investigate this axis in vitro. RESULTS: First, we studied whether gut commensals are involved in Reg3 expression in mice, and found that antibiotic-mediated reduction of Clostridia downregulated intestinal Reg3B. A loss in Clostridia was accompanied by a significant reduction of short-chain fatty acids [SCFAs], and knock-out [KO] mice for SCFA receptors GPR43 and GPR109 expressed less intestinal Reg3B/-G. Propionate was found to induce Reg3 in intestinal organoids and in gnotobiotic mice colonized with a defined, SCFA-producing microbiota. Investigating the role of Reg3B as a protective factor in colitis, we found that Reg3B-KO mice display increased inflammation and less crypt proliferation in the DSS colitis model. Propionate decreased colitis and increased proliferation. Treatment of organoids exposed to DSS with Reg3B or propionate reversed the chemical injury with a loss of expression of the stem-cell marker Lgr5 and Olfm4. CONCLUSIONS: Our results suggest that Clostridia can regulate Reg3-associated epithelial homeostasis through propionate signalling. We also provide evidence that the Reg3-propionate axis may be an important mediator of gut epithelial regeneration in colitis.