Impact of Tissue Expander Surface Texture on Two-Stage Breast Reconstruction Outcomes: A Combined Analysis of Incidence, Timing, and Severity.

BACKGROUND: With ongoing investigations of the impact of device texturing on breast implant-related anaplastic large cell lymphoma (BIA-ALCL), studies have begun comparing complications profiles of tissue expanders. However, there is a paucity of timing and severity data of complications. The aim of this study is to provide a comparative survival analysis of post-operative complications between smooth (STE) and textured tissue expanders (TTE) in breast reconstruction. METHODS: A single institution experience with tissue expander breast reconstruction was reviewed for complications up to 1 year post 2nd stage reconstruction from 2014-2020. Demographics, comorbidities, operation-related variables, and complications were evaluated. Kaplan-Meier curves, cox proportional hazard models, and a consensus based ordinal logistic regression model were used to compare complication profiles. RESULTS: Of 919 ttal patients, 65.3% (n=600) received TTEs and 34.7% (n=319) received STEs. There was increased risk of infection (p<0.0001), seroma (p=0.046), expander malposition (p<0.0001), and wound dehiscence (p=0.019) in STEs compared to TTEs. However, there were also decreased risk of capsular contracture (p=0.005) in STEs compared to TTEs. Failure of breast reconstruction (p<0.001) and wound dehiscence (p=0.018) occurred significantly earlier in STEs compared to TTEs. Predictors for significantly higher severity complications included: smooth tissue expander use (p=0.007), shorter time to complication (p<0.0001), higher BMI (p=0.005), smoking history (p=0.025), and nipple sparing mastectomy (p=0.012). CONCLUSIONS: Differences in the timing and severity of complications contribute to the safety profiles of tissue expanders. STEs are associated increased odds of higher severity and earlier complications. Therefore, tissue expander selection may depend on underlying risk factors and severity predictors.

CNS lymphatic drainage and neuroinflammation are regulated by meningeal lymphatic vasculature.

Neuroinflammatory diseases, such as multiple sclerosis, are characterized by invasion of the brain by autoreactive T cells. The mechanism for how T cells acquire their encephalitogenic phenotype and trigger disease remains, however, unclear. The existence of lymphatic vessels in the meninges indicates a relevant link between the CNS and peripheral immune system, perhaps affecting autoimmunity. Here we demonstrate that meningeal lymphatics fulfill two critical criteria: they assist in the drainage of cerebrospinal fluid components and enable immune cells to enter draining lymph nodes in a CCR7-dependent manner. Unlike other tissues, meningeal lymphatic endothelial cells do not undergo expansion during inflammation, and they express a unique transcriptional signature. Notably, the ablation of meningeal lymphatics diminishes pathology and reduces the inflammatory response of brain-reactive T cells during an animal model of multiple sclerosis. Our findings demonstrate that meningeal lymphatics govern inflammatory processes and immune surveillance of the CNS and pose a valuable target for therapeutic intervention.