Expression of tumour necrosis factor-alpha in the rat dental follicle

Wise, Gary E.; Yao, Shaomian

doi:10.1016/s0003-9969(02)00153-x

Cited by 31 publications

(27 citation statements)

References 54 publications

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“…Several studies have attempted to elucidate the role of mediators of the inflammatory process on the mechanisms controlling the appearance of osteoclasts at compression sites and consequent osteoclast-dependent tooth movement (Brezniak and Wasserstein, 2002;Kohno et al, 2003;Jager et al, 2005). Previous studies showed that TNF-␣, a pro-inflammatory cytokine, might be associated with osteoclast differentiation (Abu-Amer et al, 2000;Azuma et al, 2000) and bone remodeling (Horowitz et al, 2001;Wise and Yao, 2003). The present study aimed to investigate the role of the TNFRI in controlling the production of chemokines and osteoclast and tooth movement after the application of orthodontic force in mice.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous substancessuch as hormones, cytokines, growth factors, and bone matrix constituents-are involved with osteoclastogenesis (Boyle et al, 2003;Kohno et al, 2003;Teitelbaum, 2007). For example, pro-inflammatory cytokines, such as TNF-␣, are thought to play a role in bone remodeling (Horowitz et al, 2001;Wise and Yao, 2003) and osteoclast differentiation (Azuma et al, 2000). In rats (Ogasawara et al, 2004) and in humans (Basaran et al, 2006), orthodontic tooth movement increases the levels of TNF-␣ in the periodontal tissues.…”

Section: Introductionmentioning

confidence: 99%

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The Role of Tumor Necrosis Factor Receptor Type 1 in Orthodontic Tooth Movement

Andrade

Silva

et al. 2007

J Dent Res

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Orthodontic tooth movement is dependent on osteoclast activity. Tumor necrosis factor (TNF)-alpha plays an important role, directly or via chemokine release, in osteoclast recruitment and activation. This study aimed to investigate whether the TNF receptor type 1 (p55) influences these events and, consequently, orthodontic tooth movement. An orthodontic appliance was placed in wild-type mice (WT) and p55-deficient mice (p55(-/-)). Levels of TNF-alpha and 2 chemokines (MCP-1/CCL2, RANTES/CCL5) were evaluated in periodontal tissues. A significant increase in CCL2 and TNF-alpha was observed in both groups after 12 hrs of mechanical loading. However, CCL5 levels remained unchanged in p55(-/-) mice at this time-point. The number of TRAP-positive osteoclasts in p55(-/-) mice was significantly lower than that in WT mice. Also, there was a significantly smaller rate of tooth movement in p55(-/-) mice. Analysis of our data suggests that the TNFR-1 plays a significant role in orthodontic tooth movement that might be associated with changes in CCL5 levels.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Role of Tumor Necrosis Factor Receptor Type 1 in Orthodontic Tooth Movement

Andrade

Silva

et al. 2007

J Dent Res

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“…In addition to BMP-2, this study reveals that the expression of BMP-3 in the DF is increased at day 3 and is subsequently and incrementally increased until day 9 (Fig. 1), which correlates with the expression of TNF-α (11). In conjunction with the in vivo correlation, this study reveals that TNF-α could significantly enhance the expression of BMP-3 in vitro in the DFCs (Fig.…”

Section: Discussionmentioning

confidence: 57%

“…In turn, this could promote the bone formation at the base of the crypt that is needed for tooth eruption. Paralleling this is increased expression of TNF-α in the DF at day 3 with the maximal expression at day 9 (11). This study showed that TNF-α can stimulate the expression of BMP-2 in the DFCs (Figs.…”

Section: Discussionmentioning

confidence: 85%

“…We have proposed that the DF regulates this secondary burst of osteoclastogenesis by increasing its expression of vascular endothelial growth factor (VEGF) and TNF-α (10–13), as well as by increasing its expression of receptor activator for nuclear factor κ B ligand (RANKL) (14). VEGF, which is upregulated by TNF-α (11), can substitute for CSF-1 to upregulate osteoclastogenesis in the RANK-RANKL interaction pathway by enhancing receptor activator for nuclear factor κ B (RANK) gene expression in osteoclast precursors (13). In addition, TNF-α may directly promote osteoclastogenesis via a RANK-RANKL independent pathway (15).…”

Section: Introductionmentioning

confidence: 99%

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TNF-α Upregulates Expression of BMP-2 and BMP-3 Genes in the Rat Dental Follicle—Implications for Tooth Eruption

Yao¹,

Prpić²,

Pan³

et al. 2010

Connective Tissue Research

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The dental follicle appears to regulate both the alveolar bone resorption and bone formation needed for tooth eruption. Tumor necrosis factor-alpha ( TNF-α) gene expression is maximally upregulated at postnatal day 9 in the rat dental follicle of the 1st mandibular molar, a time that correlates with rapid bone growth at the base of the tooth crypt, as well as a minor burst of osteoclastogenesis. TNF-α expression is correlated with the expression of bone morphogenetic protein-2 (BMP-2), a molecule expressed in the dental follicle that can promote bone formation. Because BMP-2 signaling may be augmented by bone morphogenetic protein-3 (BMP-3), it was the objective of this study to determine 1) if the dental follicle expresses BMP-3 and 2) if TNF-α stimulates the dental follicle cells to express BMP-2 and BMP-3. Dental follicles were collected from different postnatal ages of rat pups. Dental follicle cells were incubated with TNF-α to study its dosage and time-course effects on gene expression of BMP-2 and BMP-3, as determined by real-time RT-PCR. Next, immunostaining was conducted to confirm if the protein was synthesized and ELISA of the conditioned medium was conducted to determine if BMP-2 was secreted. We found that BMP-3 expression is correlated with the expression of TNF-α in the dental follicle and TNF-α significantly increased BMP-2 and BMP-3 expression in vitro. Immunostaining and ELISA showed that BMP-2 and BMP-3 were synthesized and secreted. This study suggests that TNF-α can upregulate the expression of bone formation genes that may be needed for tooth eruption.

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Cinnamic Acid and Cinnamaldehyde Ameliorate Cisplatin-Induced Splenotoxicity in Rats

El‐Raouf

El-Sayed

Manie

2015

J Biochem Mol Toxicol

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Cinnamic acid (CA) and cinnamaldehyde (CD) are major constituents of cinnamon species. They possess various pharmacological properties of which their antioxidant activity is a prime one. This study aims to investigate potential protective effects against cisplatin (CP)-induced splenotoxicity in rats. A single dose of CP (5 mg/kg) injected i.p. caused a significant decrease in hemoglobin content (18%), total leucocytic count (46%), neutrophils (78%), and catalase (CAT) splenic activity (64%) with a marked increase in lymphocytes (26%) and splenic content of malondialdehyde (68%) and TNF-α (69%) as compared with the control group. Contrarily, CA (50 mg/kg, p.o.) or CD (40 mg/kg, p.o.) administration for 7 days before CP ameliorated CP-induced splenotoxicity as indicated by mitigation of the biochemical parameters and histopathological changes. These results revealed the promising protective effects of CA and CD on CP-induced splenotoxicity in rats; an effect that might be attributed to antioxidant and anti-inflammatory activities.

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Expression of tumour necrosis factor-alpha in the rat dental follicle

Cited by 31 publications

References 54 publications

The Role of Tumor Necrosis Factor Receptor Type 1 in Orthodontic Tooth Movement

The Role of Tumor Necrosis Factor Receptor Type 1 in Orthodontic Tooth Movement

TNF-α Upregulates Expression of BMP-2 and BMP-3 Genes in the Rat Dental Follicle—Implications for Tooth Eruption

Cinnamic Acid and Cinnamaldehyde Ameliorate Cisplatin-Induced Splenotoxicity in Rats

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