MATERIALS AND METHODS: Twenty-four healthy male Wistar rats (R. norvegicus) were randomly divided into four groups: K1: blank, without treatment; K2: rats with an activated MEMF and PBS; P1: rats with an activated MEMF and HUCMSC-S; and P2: rats with an inactivated MEMF and HUCMSC-S. MEMF experimental animals was performed by applying a force of 0.42 N using a loop and observed for 28 days. The HUCMSC-S single dose was 2 x 106 cells (equivalent to 5 x 105 cells in 50 μl of aMEM) every two days application. After 28 days, the maxillary containing the midpalatal suture were harvested. Immunohistochemical analysis was performed to quantify the positive expression of BMP-2, BMP-4, BMP-7, VEGF, TGF-β, IGF-1 and FGF-2.
RESULTS: HUCMSC-S local application during active expansion (Group P1) significantly upregulated the expression of BMP-2, BMP-4, BMP-7, VEGF, TGF-β, IGF-1, and FGF-2 in the midpalatal suture on day 28 compared to the control groups (P ≤ 0.05).
CONCLUSION: HUCMSC-S local application effectively stimulates osteoblastogenesis and angiogenesis markers in the midpalatal suture during MEMF.
MATERIALS AND METHODS: Twenty-eight healthy male Wistar rats, 1-2 months old and 250-300 g body weight, were divided into seven groups, namely K1: control group; K2: 100 μl LPS; K3: hyperglycemia (≥230 mg/dL); K4: 100 μl LPS with hyperglycemia; K5: LPS, hyperglycemia, and 100 μl NEP; K6: LPS, hyperglycemia, and 100 μl HUCMSCS; and K7: LPS, hyperglycemia, and 100 μl HUCMSCS and NEP. Escherichia coli`s LPS was used to induce osteolysis on the calvaria. NEP and HUCMSCS were formulated and collected, then injected subcutaneously on the calvaria. Hyperglycemia-induced streptozotocin 30 mg/kg injection for one week, intraperitoneally. All samples were sacrificed on day 8. Blood samples were collected to examine TRAP and Ctsk levels with enzyme-linked immunosorbent assay. NFATc1, sclerostin, and RANK-RANKL-OPG expression investigated with immunohistochemistry.
RESULTS: HUCMSCS and NEP administration inhibit TRAP and Ctsk levels, reduce NFATc1, sclerostin, and RANK-RANKL, but enhance OPG expression in LPS-induced osteolysis with hyperglycemia with significant differences between groups (P ≤ 0.05).
CONCLUSION: HUCMSCS and NEP post-administration reduced osteoclastogenesis in LPS-induced osteolysis calvaria with hyperglycemic in rats in the early phase of bone remodelling.