Polyacrylamide gel migration after injection for breast augmentation: A case report

Polyacrylamide hydrogel (PAAG) was once considered a safe, reliable, and compatible injected filler and was widely used in breast augmentation, rhinoplasty, and other cosmetic surgeries. However, numerous complications, such as implant migration, have been observed after PAAG injections. Herein, we report a rare case of distant implant migration after PAAG injection for breast augmentation in which the material became displaced along the abdominal wall to the perineum and pelvic extraperitoneal space. After a well-prepared preoperative evaluation involving magnetic resonance imaging (MRI) and computed tomography (CT) examinations and three-dimensional hologram, debridement surgery was performed to remove the injected material. After the operation, the patient was followed up for two years and was not scheduled for a second operation. Postoperative complications of breast augmentation after PAAG injection, especially gel migration, still affect thousands of patients. Once material migration occurs, surgical removal becomes difficult. Early diagnosis and treatment are recommended

Vγ4 T Cells Inhibit the Pro-healing Functions of Dendritic Epidermal T Cells to Delay Skin Wound Closure Through IL-17A

Dendritic epidermal T cells (DETCs) and dermal Vγ4 T cells engage in wound re-epithelialization and skin inflammation. However, it remains unknown whether a functional link between Vγ4 T cell pro-inflammation and DETC pro-healing exists to affect the outcome of skin wound closure. Here, we revealed that Vγ4 T cell-derived IL-17A inhibited IGF-1 production by DETCs to delay skin wound healing. Epidermal IL-1β and IL-23 were required for Vγ4 T cells to suppress IGF-1 production by DETCs after skin injury. Moreover, we clarified that IL-1β rather than IL-23 played a more important role in inhibiting IGF-1 production by DETCs in an NF-κB-dependent manner. Together, these findings suggested a mechanistic link between Vγ4 T cell-derived IL-17A, epidermal IL-1β/IL-23, DETC-derived IGF-1, and wound-healing responses in the skin