Evaluation of DuraGen in preventing peridural fibrosis in rabbits

Peridural fibrosis is the scar tissue formed over the dura mater after a laminectomy. It has been implicated as a cause of persistence of pain after spinal surgery and associated with increased risk of complications during revision surgery. The application of a mechanical barrier to cover the peridural space to block the migration of inflammatory cells from superficial layers to the epidural space can potentially prevent or decrease scar formation. The authors evaluated the use of DuraGen for this purpose. Seventeen New Zealand White rabbits underwent bilateral L-4 and L-7 laminectomies. Each space was randomly assigned to either receive DuraGen, fat graft, or no (sham) treatment. At a mean 18 +/- 4 weeks after surgery, the animals underwent magnetic resonance (MR) imaging with and without Gd enhancement, and the area of the scar tissue overlying the middle of the laminectomy was measured. The rabbits were killed and the spinal cords with an intact dural covering were harvested. The midsection of each treated level was evaluated histologically and the scar area was measured. In rabbits in which a fat graft was placed, MR imaging of the epidural space demonstrated a significant (p < 0.05) increase in the mean area (0.9713 mm2) of scar tissue compared with those in which DuraGen was used (0.687 mm2) or those receiving sham treatment (0.6661 mm2). The same correlation was observed when the histological sections were measured at the middle of the laminectomy site where the mean areas of both DuraGen (1008 mm2) and control (2249 mm2) groups were significantly lower than that in the fat graft group (6007 mm2) (p < 0.01 and 0.05, respectively). No significant differences between the DuraGen and control groups were observed. The authors demonstrated that peridural scarring formed in all groups. The mean area of scar deposition was significantly higher in the fat graft group than in the DuraGen or control group both on MR imaging and histological analysis. DuraGen was more effective than a fat graft in preventing epidural fibrosis but not significantly different from that occurring in control animals

Recombinant Amelogenin Regulates the Bioactivity of Mouse Cementoblasts in Vitro

Amelogenin (AMG) is a cell adhesion molecule that has an important role in the mineralization of enamel and regulates events during dental development and root formation. The purpose of the present study was to investigate the effects of recombinant human AMG (rhAMG) on mineralized tissue-associated genes in cementoblasts. Immortalized mouse cementoblasts (OCCM-30) were treated with different concentrations (0.1, 1, 10, 100, 1000, 10,000, 100,000 ng · mL-1) of recombinant human AMG (rhAMG) and analyzed for proliferation, mineralization and mRNA expression of bone sialoprotein (BSP), osteocalcin (OCN), collagen type I (COL I), osteopontin (OPN), runt-related transcription factor 2 (Runx2), cementum attachment protein (CAP), and alkaline phosphatase (ALP) genes using quantitative RT-PCR. The dose response of rhAMG was evaluated using a real-time cell analyzer. Total RNA was isolated on day 3, and cell mineralization was assessed using von Kossa staining on day 8. COL I, OPN and lysosomal-associated membrane protein-1 (LAMP-1), which is a cell surface binding site for amelogenin, were evaluated using immunocytochemistry. F-actin bundles were imaged using confocal microscopy. rhAMG at a concentration of 100,000 ng · mL-1 increased cell proliferation after 72 h compared to the other concentrations and the untreated control group. rhAMG (100,000 ng · mL-1) upregulated BSP and OCN mRNA expression levels eightfold and fivefold, respectively. rhAMG at a concentration of 100,000 ng · mL-1 remarkably enhanced LAMP-1 staining in cementoblasts. Increased numbers of mineralized nodules were observed at concentrations of 10,000 and 100,000 ng · mL-1 rhAMG. The present data suggest that rhAMG is a potent regulator of gene expression in cementoblasts and support the potential application of rhAMG in therapies aimed at fast regeneration of damaged periodontal tissue., A protein with its roots in dental development stimulates the proliferation and gene expression of cells linked to regeneration. Amelogenin is a mediator of enamel and tooth root formation, and the main component of a recently-developed medicine for periodontal regeneration. An international research group led by Sema Hakki, of Selcuk University, Turkey, has now elucidated the effects of amelogenin on cementoblasts, a type of cell responsible for producing the vital, mineralized layer on surface of the tooth root. Hakki’s team found that the bacteria-derived amelogenin increased the rate of mouse cementoblast proliferation and mineralization in vitro, and increased the expression of genes related to bone and tissue generation. The team also demonstrated the presence of a likely amelogenin receptor on the cells used in their study. These findings support further investigation into amelogenin’s therapeutic potential.PubMedWoSScopu