Osteoclastogenesis In Rats Research Articles

Wheat seeds can delay orthodontic tooth movement by blocking osteoclastogenesis in rats.

BackgroundThe hormone estrogen can prevent osteoclast differentiation and suppress osteoclastic activity, which can prevent tooth relapse movement. Wheat seeds are a natural material containing phytoestrogens with similar characteristics to estrogen.ObjectiveThis study intends to determine the influence of wheat seeds in reducing osteoclastogenesis following orthodontic tooth movement (OTM).Materials and methodsForty male Sprague Dawley rats were used in this experimental study. The rats were divided into control and treatment groups (n=20). In both groups, the rat maxillary incisors were moved distally using a 0.012 U stainless steel orthodontic appliance with a 2 mm diameter coil and 5 mm wire length. The treatment group received wheat seeds at a dose of 0.6 gram/day. The animals were sacrificed at days 0, 1, 7, and 14 after using the orthodontic appliance (4 subgroups according to observations of days; n=5). RANKL and OPG expressions were determined from the gingival crevicular fluid (GCF) samples using ELISA analysis. Statistical analysis of the data collected was calculated with the independent sample t-test (P<0.05).ResultsAll the experimental procedures were well-tolerated and did not change the animals’ weight. On days 7 and 14, the OTM rate of the treatment group was significantly lower than the control group (P<0.05). ELISA test results showed that the OPG level was significantly higher on days 1, 7, and 14, while the RANKL level was considerably lower on day 14 in the wheat seeds group compared with the control group (P<0.05).ConclusionWheat seeds can promote osteoclastogenesis inhibition and delay OTM.

Cocoa administration may accelerate orthodontic tooth movement by inducing osteoclastogenesis in rats.

Objective(s):To investigate the effect of cocoa on orthodontic tooth movement (OTM) rate, osteoprotegerin (OPG), and receptor activator of nuclear factor κ β ligand (RANKL) levels after OTM.Materials and Methods:A total of 24 Sprague-Dawley rats were included in the study. They were equally divided into two groups: cocoa and control. The upper incisors of all rats were subjected to 35 cN orthodontic force and moved distally with a stainless steel 3-spin coil spring. During OTM, the cocoa group was given 4.8 g of unsweetened cocoa once a day. At 4 subsequent time points (0, 1, 7, and 14 days), the OTM rate was determined by measuring the distance between the mesial tips using a digital caliper, while OPG and RANKL levels were examined based on their gingival crevicular fluid through specific enzyme-linked immunosorbent assay (ELISA). Data gathered were analyzed through independent t-test (P<0.05).Results:The OTM rate of the cocoa group was significantly higher than that of the control group on days 1, 7, and 14 (P<0.05). ELISA analysis revealed that the OPG level was significantly lower on day 14. Furthermore, the RANKL level was significantly higher on days 0, 1, and 7 for the cocoa group compared with the control group (P<0.05).Conclusion:These results indicate that cocoa has the potential effect to modulate the OTM rate by inducing osteoclastogenesis, which suppresses the OPG level and stimulates the RANKL level, in rats.

Methotrexate Chemotherapy Promotes Osteoclast Formation in the Long Bone of Rats via Increased Pro-Inflammatory Cytokines and Enhanced NF-κB Activation

Cancer chemotherapy with methotrexate (MTX) is known to cause bone loss. However, the underlying mechanisms remain unclear. This study investigated the potential role of MTX-induced pro-inflammatory cytokines and activation of NF-κB in the associated osteoclastogenesis in rats. MTX (0.75 mg/kg per day) was administered for 5 days, and bone and bone marrow specimens were collected on days 6, 9, and 14. Compared with a normal control, MTX increased the density of osteoclasts within the metaphyseal bone and the osteoclast formation potential of marrow cells on day 9. RT-PCR analysis of mRNA expression for pro-osteoclastogenic cytokines in the metaphysis indicated that, although the receptor activator of NF-κB ligand/osteoprotegerin axis was unaffected, expression of tumor necrosis factor (TNF)-α, IL-1, and IL-6 increased on day 9. Enzyme-linked immunosorbent assay analysis of plasma showed increased levels of TNF-α on day 6 and of IL-6 on day 14. Plasma from treated rats induced osteoclast formation from normal bone marrow cells, which was attenuated by a TNF-α-neutralizing antibody. Indicative of a role for NF-κB signaling, plasma on day 6 increased NF-κB activation in RAW(264.7) cells, and plasma-induced osteoclastogenesis was abolished in the presence of the NF-κB inhibitor, parthenolide. Our results demonstrate mechanisms for MTX-induced osteoclastogenesis and show that MTX induces osteoclast differentiation by generating a pro-osteoclastogenic environment in both bone and the circulation, specifically with increased TNF-α levels and activation of NF-κB.

Liposomes containing phosphatidylserine inhibit osteoclastogenesis in rats

Liposomes containing phosphatidylserine inhibit osteoclastogenesis in rats

Curcumin suppresses increased bone resorption by inhibiting osteoclastogenesis in rats with streptozotocin-induced diabetes

Curcumin is a potent inhibitor of the transcription factor activator protein-1 which plays an essential role in osteoclastogenesis. However, the effects of curcumin on bone metabolism have not been clarified in vivo. We reported herein the inhibitory effects of curcumin on the stimulated osteoclastic activity in insulin-dependent diabetes mellitus using rats with streptozotocin-induced diabetes. A dietary supplement of curcumin reversed the increase in levels of activity and mRNA of tartrate-resistant acid phosphatase (TRAP) and cathepsin K to control values. A histochemical analysis showed that the increase in TRAP-positive cells in the distal femur of the diabetic rats was reduced to the control level by the supplement. These results suggested that curcumin reduced diabetes-stimulated bone resorptive activity and the number of osteoclasts. When bone marrow cells were cultured with macrophage colony stimulating factor and receptor activator NF-κB ligand (RANKL), the increased activity to form TRAP-positive multinucleated cells and the increased levels of mRNA and protein of c-fos and c-jun in the cultured cells from diabetic rats decreased to control levels in the curcumin-supplemented rats. Similarly, the increased expression of c-fos and c-jun in the distal femur of the diabetic rats was significantly reduced by the supplement. These results suggested that curcumin suppressed the increased bone resorptive activity through the prevention of osteoclastogenesis associated with inhibition of the expression of c-fos and c-jun in the diabetic rats.