| Various methods for treatment of auricular defects are known. The most common way of auricle reconstruction is the use of autogenous rib cartilage. But costal cartilage autograft will cause such poor surgical consequences as absorption, deformation, contracture in long-term following-up period. Transforming growth factor-β1 (TGF-(31) is one of the important growth factors which regulate the proliferation and metabolism of cartilage. TGF-β1 is confirmed to stimulate proliferation of chondrocytes, and increase synthesis of proteoglycans and type II collagen in vitro. There is no reported about how TGF-β1 works to costal cartilage autograft in vivo.Objective:To evaluate the function of TGF-β1 to costal cartilage autograft in proliferation and metabolism in vivo.Materials and MethodsExperimental animals and groups:There are totally 36 healthy New Zealand white rabbits, whose sex is not care.18 of them are young (1 month in age, lkg in weight), and the others are adult (6 month in age,2kg in weight). All of them are divided into young group and adult group by age. In each group, the rabbits were randomly divided into 6 groups:FG control group,5ng/ml TGF-β1+FG group, 10ng/ml TGF-β1+FG group, surgical control group, 5ng/ml TGF-β1+NS group, 10ng/ml TGF-β1+NS group, with 3 rabbits in each group.Methods:Firstly, the rabbits are anesthetized and sterilized. Then 2 pieces of the eighth costal cartilage are taken, and 2 pieces respectively from the seventh and ninth costal cartilage are removed. The cartilage tissue is combined with the perichondrium and is 1cm in long. Finally, in different groups, four pieces of cartilage are implanted respectively into the subcutaneous chamber of the rabbit back, directly or with FG or with the injection of TGF-β1. After 8 weeks, the autografted and physiological costal cartilage are removed. The multiplication, the degeneration and the cells viability of cartilage cells were observed with hematoxylin and eosin staining and toluidine blue staining, microstructure of chondrocyte were observed under the transmission electron microscope (TEM),and hydroxyproline(HYP) and glycosaminoglycan (GAG) content were measured.ResultsUnder this experimental condition, in young groups, the chondrocyte proliferate most actively in the 10 ng/ml TGF-β1+FG group,the content of hydroxyproline and GAG, which are similar with the blank control group (P> 0.05), are significantly higher than other groups (P< 0.05),and the difference was statistically significant.In the adult groups, the degeneration of chondrocytes has been observed in every group and extracellular matrix is decreased obviously.The effect of TGF-β1 is not significant to the costal cartilage autograft.Conclusions1. In the young groupsTGF-β1 promotes the proliferation of chondrocytes and maintains their synthesis of specific matrix. TGF-β1 can obviously inhibit apoptosis and necrosis of chondrocytes. The effect of lOng/ml TGF-β1 is superior to the effect of 5ng/ml TGF-β1. In the TGF-β1+FG group, FG as the carrier of TGF-β1 has certain slow-released effect to TGF-β1 and can delay the degradation of TGF-β1, so that FG enhances the ability that TGF-β1 induces chondrocyte multiplication.2. In the adult groupsComparing with the youth groups, the degeneration of chondrocytes has been observed in every adult group and extracellular matrix is decreased obviously.The effect of TGF-β1 to the cartilage grafts is not obvious. Only 10ng/ml TGF-β1+FG had inhibitory effect in degradation of matrix, which shows that the cartilage grafts may still retain the ability to respond to TGF-β1.3. TGF-β1 can maintain the structure and function of cartilage autografts in vivo, especially to the youth group. |
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