Presentation and Management of Silicone Lymphadenopathy: A Single Institutional Retrospective Cohort Study

Silicone Lymphadenopathy (SL) is a complication of breast implants that involves migration of silicone to nearby soft tissue/lymph nodes. Data on its clinical features and management is scarce. We aimed to identify the clinical presentation and management of SL.INTRODUCTIONSilicone Lymphadenopathy (SL) is a complication of breast implants that involves migration of silicone to nearby soft tissue/lymph nodes. Data on its clinical features and management is scarce. We aimed to identify the clinical presentation and management of SL.A single-institution retrospective cohort study was conducted from our institutional imaging system where search terms "Silicone lymphadenopathy", "silicone adenitis" and "silicone adenopathy" were used to identify patients with SL (January 2016-September 2023). Patient demographics, clinical features, imaging findings, pathological investigation, and treatment were obtained from the medical records.METHODSA single-institution retrospective cohort study was conducted from our institutional imaging system where search terms "Silicone lymphadenopathy", "silicone adenitis" and "silicone adenopathy" were used to identify patients with SL (January 2016-September 2023). Patient demographics, clinical features, imaging findings, pathological investigation, and treatment were obtained from the medical records.Of 52 patients with SL, breast augmentation accounted for 90.4% of the implant placements. All patients had silicone implants placed at some time. A significant portion of patients (69.3%) were asymptomatic, while 7.7% had non-tender lymphadenopathy, 19.2% experienced painful lymphadenopathy, and 1.9% presented with mixed symptoms. Implant rupture was observed in 88.7% of cases; 13.0% intracapsular, 26.1% extracapsular, 15.2% both, and unknown in 45.7%. Axillary nodes were the most commonly involved (86.5%), and ultrasonography was most commonly used to detect SL (80.7%). Biopsy was performed in 17.3% of cases, confirming benign pathology in all cases. No patients required surgical excision of lymph nodes for management of SL.RESULTSOf 52 patients with SL, breast augmentation accounted for 90.4% of the implant placements. All patients had silicone implants placed at some time. A significant portion of patients (69.3%) were asymptomatic, while 7.7% had non-tender lymphadenopathy, 19.2% experienced painful lymphadenopathy, and 1.9% presented with mixed symptoms. Implant rupture was observed in 88.7% of cases; 13.0% intracapsular, 26.1% extracapsular, 15.2% both, and unknown in 45.7%. Axillary nodes were the most commonly involved (86.5%), and ultrasonography was most commonly used to detect SL (80.7%). Biopsy was performed in 17.3% of cases, confirming benign pathology in all cases. No patients required surgical excision of lymph nodes for management of SL.Most patients with SL are asymptomatic and are managed with observation. Biopsy and surgical intervention should be reserved for those patients with abnormal imaging or persistent symptoms. Evaluation of lymphadenopathy is essential to exclude malignancy in patients with a history of breast cancer.CONCLUSIONMost patients with SL are asymptomatic and are managed with observation. Biopsy and surgical intervention should be reserved for those patients with abnormal imaging or persistent symptoms. Evaluation of lymphadenopathy is essential to exclude malignancy in patients with a history of breast cancer.This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .LEVEL OF EVIDENCE IIIThis journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266

Evaluation of Porcine-Derived Collagen Membranes for Soft Tissue Augmentation in the Oral Cavity: An In Vivo Study

The use of porcine-derived collagen membranes (PDCM) to improve intraoral soft tissue rehabilitation remains under investigation. Different degrees of crosslinking have yielded differences in resorption time and inflammation surrounding collagen membranes. The aim of this study was to evaluate the in vivo performance of bilayered PDCMs with varying degrees of crosslinking for the regeneration of oral soft tissue defects. Bilateral split-thickness oral mucosa defects were created in mandibles of beagles (n=17) and assigned to one of the following: bilayer PDCM (high crosslinking porcine dermis in sheet form—H-xlink) and (low crosslinking porcine dermis in sheet form—L-xlink), bilayer PDCM (non-crosslinked predicate collagen membrane in spongy form—Ctrl), or negative control (Sham) and compared with positive control (unoperated). Animals were euthanized after 4-, 8-, or 12-weeks of healing to evaluate soft tissue regeneration and remodeling through histomorphometric analyses. H-xlink membranes presented delayed healing with a poorly developed epithelial layer (analogous to the sham group) across time points. Relative to Ctrl at 8 and 12 weeks, defects treated with H-xlink presented no difference in semiquantitative scores ( P > 0.05), while L-xlink exhibited greater healing ( P = 0.042, P = 0.043, at 8 and 12 weeks, respectively). Relative to positive control, L-xlink exhibited similar healing at 8 weeks and greater healing at 12 weeks ( P = 0.037) with a well-developed epithelial layer. Overall, groups treated with L-xlink presented with greater healing relative to the positive control after 12 weeks of healing and may serve as an alternative to autologous grafts for intraoral soft tissue regeneration

Effect of Porcine-Derived Collagen Membrane Crosslinking on Intraoral Soft Tissue Augmentation: A Canine Model

Peri-implant disease and gingival recession may be partially attributed to inadequate keratinized tissue. Soft tissue augmentation procedures utilizing non-autologous biomaterials, such as porcine-derived collagen membranes, have been gaining prominence and exogenous crosslinking is being actively investigated to improve the collagen membrane’s stability and potential for keratinized tissue gain. The aim of this preclinical study was to evaluate the performance of a novel, crosslinked porcine collagen membrane (ZdermTM, Osteogenics Biomedical, Lubbock, TX, USA) relative to an established, commercially available, non-crosslinked counterpart (Mucograft®, Geistlich Pharma North America Inc., Princeton, NJ, USA) in a canine mandibular model. Bilateral split-thickness mucosal defects were created in adult beagles (n = 17), with each site receiving one membrane. Qualitative and quantitative histomorphometric analyses of groups were performed after 4, 8, and 12 weeks of healing and compared to unoperated, positive controls from the same subject. No significant differences in membrane presence were observed between ZdermTM and Mucograft® at 4, 8, and 12 weeks of permitted healing (p > 0.05). Similarly, the average keratinized tissue (KT) length between ZdermTM and Mucograft® groups was statistically equivalent across all healing times (p > 0.05). However, qualitative histological evaluation revealed greater rete ridge morphology amongst defects treated with ZdermTM in comparison to Mucograft®. Nevertheless, both membranes exhibited excellent biocompatibility and are well-suited for soft tissue augmentation procedures in the oral cavity

Neuropilin 1 regulates bone marrow vascular regeneration and hematopoietic reconstitution

AbstractIonizing radiation and chemotherapy deplete hematopoietic stem cells and damage the vascular niche wherein hematopoietic stem cells reside. Hematopoietic stem cell regeneration requires signaling from an intact bone marrow (BM) vascular niche, but the mechanisms that control BM vascular niche regeneration are poorly understood. We report that BM vascular endothelial cells secrete semaphorin 3 A (SEMA3A) in response to myeloablation and SEMA3A induces p53 – mediated apoptosis in BM endothelial cells via signaling through its receptor, Neuropilin 1 (NRP1), and activation of cyclin dependent kinase 5. Endothelial cell – specific deletion of Nrp1 or Sema3a or administration of anti-NRP1 antibody suppresses BM endothelial cell apoptosis, accelerates BM vascular regeneration and concordantly drives hematopoietic reconstitution in irradiated mice. In response to NRP1 inhibition, BM endothelial cells increase expression and secretion of the Wnt signal amplifying protein, R spondin 2. Systemic administration of anti - R spondin 2 blocks HSC regeneration and hematopoietic reconstitution which otherwise occurrs in response to NRP1 inhibition. SEMA3A – NRP1 signaling promotes BM vascular regression following myelosuppression and therapeutic blockade of SEMA3A – NRP1 signaling in BM endothelial cells accelerates vascular and hematopoietic regeneration in vivo.</jats:p