Role of bariatric surgery in reducing periprosthetic joint infections in total knee arthroplasty. A systematic review and meta-analysis.

BACKGROUND: Obesity represents an epidemic of rising numbers worldwide year after year. In the Orthopedic field, obesity is one of the major causes leading to osteoarthritis needing Total Joint Arthroplasty (TJA). Still, contextually, it represents one of the most significant risk factors for joint replacement complications and failures. So, bariatric Surgery (BS) is becoming a valuable option for weight control and mitigating obesity-related risk factors. This review of the literature and meta-analysis aims to evaluate periprosthetic joint infections (PJI) and surgical site infections (SSI) rates in patients who underwent TKA after BS compared to obese patients without BS. METHODS: Systematic review was performed according to Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines up to October 2023. We included longitudinal studies comparing obese patients who underwent total knee arthroplasty after bariatric surgery (study group) and obese patients who underwent TKA (control group). The surgical site infection and Periprosthetic joint infection rate were compared among groups using a meta-analytical approach. RESULTS: The online database and references investigation identified one hundred and twenty-five studies. PJI rate differed significantly among groups, (z = -21.8928, p < 0.0001), with a lower risk in the BS group (z = -10.3114, p < 0.0001), for SSI, instead, not statistically significance were recorded (z = -0.6784, p = 0.4975). CONCLUSIONS: The current Literature suggests that Bariatric Surgery can reduce infectious complications in TKA, leading to better outcomes and less related costs treating of knee osteoarthritis in obese patients.

Defective function of Fas in patients with type 1 diabetes associated with other autoimmune diseases.

Fas (CD95) triggers programmed cell death and is involved in cell-mediated cytotoxicity and in shutting off the immune response. Inherited loss-of-function mutations hitting the Fas system cause the autoimmune/lymphoproliferative syndrome (ALPS). We have recently shown that ALPS patients' families display increased frequency of common autoimmune diseases, including type 1 diabetes. This work evaluates Fas function in type 1 diabetic patients without typical ALPS. Cell death induced by anti-Fas monoclonal antibody was investigated in T-cells from 13 patients with type 1 diabetes alone and 19 patients with type 1 diabetes plus other autoimmune diseases (IDDM-P). Moreover, we analyzed 19 patients with thyroiditis alone (TYR), because most IDDM-P patients displayed thyroiditis. Frequency of resistance to Fas-induced cell death was significantly higher in patients with IDDM-P (73%) than in type 1 diabetic (23%) or TYR (16%) patients or in normal control subjects (3%). The defect was specific because resistance to methyl-prednisolone-induced cell death was not significantly increased in any group. Fas was always expressed at normal levels, and no Fas mutations were detected in four Fas-resistant IDDM-P patients. Analysis of the families of two Fas-resistant patients showing that several members were Fas-resistant suggests that the defect has a genetic component. Moreover, somatic fusion of T-cells from Fas-resistant subjects and the Fas-sensitive HUT78 cell line generates Fas-resistant hybrid cells, which suggests that the Fas resistance is due to molecules exerting a dominant-negative effect on a normal Fas system. These data suggest that Fas defects may be a genetic factor involved in the development of polyreactive type 1 diabetes.