Low dose propranolol decreases orthodontic movement.

OBJECTIVE: Low dose propranolol has previously been demonstrated to suppress bone remodelling. Therefore, its effect on orthodontic movement was tested. DESIGN: Rats were assigned as follows (n=5): animals with no orthodontic appliance (G1); the remaining groups were fitted with a Ni-Ti closed-coil spring ligated to the upper left first molar and connected to the incisors using metal and resin and received vehicle only (G2), 0.1mg/kg (G3) or 20mg/kg (G4) of propranolol orally. Cone Beam Computed Tomography was performed using high resolution for image capture. The distance between the first and second upper molars, both with and without the orthodontic appliance, was measured in millimetres. Gingival tissue was harvested and assessed for IL-1ß and IL-6 using ELISA and for ICAM-1 and RANKL by Western blotting. RESULTS: The orthodontic appliance induced a significant tooth movement in G2 when compared to the animals without an orthodontic appliance (G1) (p<0.05). The animals from G3 showed a significantly reduction in tooth movement (p<0.05) when compared with rats from G2. Animals treated with 20mg/kg of propranolol (G4) showed tooth movement similar to that of G2. The reduced tooth movement observed in the animals treated with 0.1mg/kg of propranolol (G3) occurred due to decreased amounts of IL-1ß and IL-6, in addition to lower ICAM-1 and RANKL expression. CONCLUSIONS: Low dose propranolol inhibits bone remodelling and orthodontic movement.

Secreted osteoclastogenic factor of activated T cells (SOFAT), a novel osteoclast activator, in chronic periodontitis.

A novel activated human T cell-secreted cytokine, referred as secreted osteoclastogenic factor of activated T cells (SOFAT), that induce osteoclastogenesis in a RANKL-independent manner was recently described. This study evaluated the role of SOFAT in periodontal tissues and periodontitis. Gingival biopsies were harvested from systemically healthy non-periodontitis (n=15) and chronic periodontitis patients (n=15). The mRNA and protein levels of SOFAT were measured by qPCR and by enzyme-linked immunosorbent assay, respectively. Moreover, RAW 264.7 cells were cultured with SOFAT or Receptor activator of nuclear factor-kB ligand (RANKL) and stained for tartrate-resistant acid phosphatase (TRAP). Also, mice received a palatal injection between the first and second upper molar of SOFAT (100 ng/ml) or saline solution (0.9%). The upper jaw was removed, histologically processed and stained with hematoxilin and eosin to observe the presence of osteoclast-like cells. The mRNA and protein levels of SOFAT were significantly higher in the gingival tissue of the periodontitis group when compared to non-periodontitis one (p<0.05). In addition, SOFAT potently induced TRAP-positive multinucleated cell formation by RAW 264.7 cells as well as induced the formation of osteoclast-like cells in the periodontal ligament in mice. The present study demonstrated that SOFAT may play an important role in periodontitis.