Immunolocalization of FGF-2 and VEGF in rat periodontal ligament during experimental tooth movement

Abstract

ObjectiveThis article aimed at identifying the expression of fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF) in the tension and pressure areas of rat periodontal ligament, in different periods of experimental orthodontic tooth movement.MethodsAn orthodontic force of 0.5 N was applied to the upper right first molar of 18 male Wistar rats for periods of 3 (group I), 7 (group II) and 14 days (group III). The counter-side first molar was used as a control. The animals were euthanized at the aforementioned time periods, and their maxillary bone was removed and fixed. After demineralization, the specimens were histologically processed and embedded in paraffin. FGF-2 and VEGF expressions were studied through immunohistochemistry and morphological analysis.ResultsThe experimental side showed a higher expression of both FGF-2 and VEGF in all groups, when compared with the control side (P < 0.05). Statistically significant differences were also found between the tension and pressure areas in the experimental side.ConclusionBoth FGF-2 and VEGF are expressed in rat periodontal tissue. Additionally, these growth factors are upregulated when orthodontic forces are applied, thereby suggesting that they play an important role in changes that occur in periodontal tissue during orthodontic movement.

Orthodontic tensile strain induces angiogenesis via type IV collagen degradation by matrix metalloproteinase‐12

“…These results suggest that our method using μCT is reliable for observations of remodeling blood vessels in PDL. More importantly, we discovered that the application of orthodontic force‐induced angiogenesis in the tension zone of PDL, which is supported by the reports that the expression of angiogenic growth factors such as basic fibroblast growth factor and vascular endothelial growth factor were increased by the application of orthodontic force in the tension zone of PDL tissue . Taken together, our results suggest that the orthodontic force induces MMP‐12 expression in the tension zone, which results in the increase in Col‐IV degradation in the PDL during the early stage of OTM.…”

“…Owing to the indispensability of blood supply for the remodeling of PDL, the blood vessels are involved in the regulation of PDL remodeling . Previous studies reported the increased angiogenic factors and increased blood vessels in the tension zone of PDL during the early stage of OTM, though the regulatory mechanism is still unclear in the remodeling of blood vessels in PDL during OTM.…”

TGF-β-induced activation of conjunctival fibroblasts is modulated by FGF-2 and substratum stiffness

“…During cutaneous wound healing, FGF-2 exhibits antiscarring effects, reducing the number of myofibroblasts by antagonizing myofibroblast transdifferentiation and inducing apoptosis of myofibroblasts [15][16][17]. In addition, FGF-2 is secreted in response to mechanical stress, a factor that modulates wound healing in various tissue, such as cartilage, periodontal ligament, bone marrow, vascular smooth muscle, bladder smooth muscle, and skeletal muscle [18][19][20][21][22][23][24][25][26][27]. Although FGF-2 reportedly stimulates transforming growth factor (TGF)-β-mediated cell proliferation in subconjunctival fibroblasts directly [28], the relationships among TGF-β, FGF-2, and mechanical stress during conjunctival wound healing remain unclear.…”

MicroRNA‐195‐5p Regulates Osteogenic Differentiation of Periodontal Ligament Cells Under Mechanical Loading

“…Recent studies have shown that miR‐338 and miR‐223 regulate the osteogenic differentiation of mesenchymal stem cells by targeting FGFR2 (Guan et al, ; Liu et al, ). FGF‐2 and VEGF expression was higher at the PDL experimental TS of OTM rats than at the control side (Salomao et al, ). Moreover, FGF2 injection of rats produced stronger effects on the rate of tooth movement (Seifi, Badiee, Abdolazimi, & Amdjadi, ).…”

“…Previous studies have suggested that PDLCs can differentiate into osteoblasts when cultured under tension strain (Pinkerton et al, ; Shen et al, ; Wei et al, ; Wescott et al, ). Osteogenic differentiation under mechanical loading is tightly regulated by multiple signaling molecules (i.e., bone morphogenetic proteins (BMPs), WNTs, and fibroblast growth factors (FGFs)) that activate osteoblast‐specific transcription factors, including runt‐related transcription factor 2 (RUNX2) and osterix (OSX), amnong others (Celeste et al, ; Lu, Duan, Zhang, Wu, & Wang, ; Salomao et al, ). However, the regulatory processes at the post‐transcriptional level are poorly characterized.…”