|
The histopathologic change and immune response, induced by porcine dermal collagen membrane(PDCM), was evaluated by Sprague-Dawley rats animal model. The PDCM, which was cross- linked by 3%, 0.05%, 0.01%, or 0% glutaraldehyde (GA) for 1 hour, was implanted into muscle tissue of S.D. rats. Following 1, 3, 5, 7, 10, 14, 21, 28, 42 days, the rats were sacrificed; PDCM with the surroundingmuscle tissue in implanted sites were prepared for (1) Hematoxylin & Eosin stain, (2) Alcian blue-PAS stain, (3) immunohistochemistry stain(avidin-biotin complex method). According to microscropic observation, the resorption rates of PDCM in vivo were: 0% GA-PDCM less than 3 weeks, 0.01% GA-PDCM less than 6 weeks, 0.05% and 3% GA-PDCM longer than 6 weeks.However, the sustenance to maintain cellular seperating effect was: 3% GA-PDCM maintaining cellular seperating effect for 21 day, and 0.05%、0.01%、0% GA- PDCM maintaining for 7 to 10 days. After this period, PDCM were invaded by fibroblasts and capillaries. PDCM could induced foreign body reaction in implanted muscle tissue, which would progressed to delayed type hypersensitivity (DTH). The intensity of induced DTH was corelated to the persistence of PDCM; the longer PDCM persised , the more intensively the DTH would be. The DTH induced by 3% GA-PDCM was most intensively and progressed to most mature reaction, but those of 0%GA-PDCM was most mild. According to the result of immunohistochemistric stain, the activated macrophages were the primary effector cells of DTH. This reaction was corelated to CD4 T lymphocytes, but not to CD8 T lymphocytes. In implanted sites, there was no significant amount of IgG、IgM antibody deposition. In other words, the possibility of PDCM inducing type II hypersensitivity was very low. According to above finding, we suggest that the immune response induced by PDCM belongesto reaction managed by T helper 1(Th 1) cells. In the furture, if PDCM is utilized in periodontal therapy, there would be not only guded tissue regenerative effect, but also changing immune response from destructive pathway to repair one,which was managed by Th 1 cells.
|