Ear reconstruction surgeries for congenital deformities and trauma are common, highlighting the need for improved cartilage regeneration. Lactoferrin (LF), a natural and cost-effective protein, is promising due to its anti-inflammatory, antimicrobial, and prochondrogenic properties. This study investigates the effects of LF on the viability, proliferation, and chondrogenesis of rabbit auricular chondrocytes. For in vitro studies, auricular chondrocytes were cultured for three passages, after which 3D pellets were formed. LF significantly increased chondrocyte metabolic activity by 1.5 times at doses of 10 and 500 μg/mL. At passage 3, LF at concentrations of 10 and 100 μg/mL increased cell proliferation rates by 2- and 1.5-fold, respectively. Immunohistochemical staining of the pellets demonstrated that LF at 10 μg/mL increased the amount of sex-determining region Y-Box Transcription Factor 9 (Sox9)+ cells by 30%, while at 100 μg/mL, it doubled the type II collagen deposits. For in vivo studies, a rabbit ear defect model was utilized. On post-operative day 60, the LF-treated group exhibited more mature cartilage regeneration, with a higher density of elastic fibers. By day 90 post-surgery, LF application led to the restoration of normal elastic cartilage throughout the defect. These findings suggest that LF promotes auricular chondrocytes chondrogenesis and could be beneficial for tissue engineering of the elastic cartilage.

Ear reconstruction surgeries, including those addressing congenital deformities like microtia and trauma-induced damages, are relatively common. Given the demand, seeking new approaches to cartilage regeneration is crucial to improving surgical outcomes, reducing recovery times, and enhancing the quality of life for patients. The natural and cost-effective protein lactoferrin (LF) draws significant attention. It is renowned for its anti-inflammatory, antimicrobial properties, and its ability to stimulate chondrogenesis of the hyaline cartilage. This study investigates the effects of LF on the viability, proliferation, and chondrogenesis of rabbit auricular chondrocytes using both in vitro and in vivo models. In vitro, LF significantly increased the metabolic activity of chondrocytes in a dose-dependent manner, with an optimal concentration of 10 μg/ml enhancing cell prolifera-tion and metabolic activity. At this concentration, it also stimulated chondrogenesis. For in vivo studies, a rabbit ear defect model was used. Macroscopic and histological analyses revealed that LF-treated groups exhibited more mature cartilage regeneration, with higher density and organi-zation of elastic fibers compared to control. These findings suggest that LF promotes auricular chondrocyte chondrogenesis and could be beneficial for tissue engineering and clinical applications in cartilage repair.