scholarly journals Relationships between tooth eruption, occlusion and alveolar bone resorption: Cytological and cytochemical studies of bone resorption on rat incisor alveolar bone facing the enamel.

1990 ◽  
Vol 53 (5) ◽  
pp. 497-509 ◽  
Author(s):  
Kazuharu IRIE
Keyword(s):  
Bone Resorption ◽  
Alveolar Bone ◽  
Tooth Eruption ◽  
Rat Incisor

Tartrate-resistant acid phosphatase in mononuclear and multinuclear cells during the bone resorption of tooth eruption.

1987 ◽  
Vol 35 (11) ◽  
pp. 1227-1230 ◽  
Author(s):  
S C Marks ◽  
M L Grolman
Keyword(s):  
Acid Phosphatase ◽  
Bone Resorption ◽  
Connective Tissue ◽  
Mononuclear Cells ◽  
Alveolar Bone ◽  
Tooth Eruption ◽  
Tartrate Resistant Acid Phosphatase ◽  
Dental Follicle ◽  
Multinuclear Cells ◽  
Cytochemical Marker

Tartrate-resistant acid phosphatase (TRAP) has been used as a cytochemical marker for the cell mediators of bone resorption, osteoclasts and their mononuclear precursors. We have applied a cytochemical method for TRAP to study the dependence of the osteoclast-mediated bone resorption of tooth eruption on the dental follicle, a connective tissue investment of the developing tooth, by analyzing the TRAP activity of mononuclear cells in the dental follicle before and during pre-molar eruption in dogs. The percentage of TRAP-positive monocyte cells increases until mid-eruption, slightly preceding a previously demonstrated rise in numbers of osteoclasts on adjacent bone surfaces. These data suggest an ontogenetic relationship between follicular mononuclear cells and osteoclasts on adjacent alveolar bone surfaces during tooth eruption. However, because TRAP occurs in other tissues and is not an exclusive indicator of pre-osteoclasts, proof of their relationship will have to await application of more definitive techniques.

PTHrP Induces Notch Signaling in Periodontal Ligament Cells

2009 ◽  
Vol 88 (6) ◽  
pp. 551-556 ◽  
Author(s):  
A. Nakao ◽  
H. Kajiya ◽  
H. Fukushima ◽  
A. Fukushima ◽  
H. Anan ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Notch Signaling ◽  
Periodontal Ligament ◽  
Alveolar Bone ◽  
Root Resorption ◽  
Tooth Eruption ◽  
Periodontal Ligament Cells ◽  
Dependent Manner ◽  
Human Pdl Cells ◽  
Pdl Cells

Periodontal ligament (PDL) cells are known to play important roles in tooth eruption and alveolar bone metabolism. We previously reported that PTHrP increases RANKL expression in human PDL cells, suggesting that it promotes odontoclastic root resorption during tooth eruption. While it is known that Notch-related genes play a key role during bone development, the role of the Notch signaling pathway in PDL cells during tooth and bone resorption is less clear. We hypothesized that PTHrP induces a Notch ligand in PDL cells and thereby regulates osteo- and odontoclastogenesis. We found that PTHrP increased Notch1 ligand Jagged1 expression in human PDL cells in a dose- and time-dependent manner. PTHrP-induced Jagged1 up-regulation was mediated by PKA activation, but not by PKC. Jagged1 also promoted RANKL-induced osteoclastogenesis. These results demonstrate that PTHrP induces Jagged1 expression in PDL cells, leading to osteo- and odontoclastogenesis, and thus likely promoting tooth and alveolar bone resorption.

scholarly journals Granulocyte colony-stimulating factor (G-CSF) mediates bone resorption in periodontitis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hui Yu ◽  
Tianyi Zhang ◽  
Haibin Lu ◽  
Qi Ma ◽  
Dong Zhao ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Alveolar Bone ◽  
Bone Volume ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Periodontal Tissues ◽  
Gingival Epithelial Cells ◽  
Trap Staining ◽  
Experimental Periodontitis ◽  
Stimulating Factor

Abstract Background Granulocyte colony-stimulating factor (G-CSF) is an important immune factor that mediates bone metabolism by regulating the functions of osteoclasts and osteoblasts. Bone loss is a serious and progressive result of periodontitis. However, the mechanisms underlying the effects of G-CSF on periodontal inflammation have yet not been completely elucidated. Here, we examined whether an anti-G-CSF antibody could inhibit bone resorption in a model of experimental periodontitis and investigated the local expression of G-CSF in periodontal tissues. Methods Experimental periodontitis was induced in mice using ligatures. The levels of G-CSF in serum and bone marrow were measured; immunofluorescence was then performed to analyze the localization and expression of G-CSF in periodontal tissues. Mice with periodontitis were administered anti-G-CSF antibody by tail vein injection to assess the inhibition of bone resorption. Three-dimensional reconstruction was performed to measure bone destruction‐related parameters via micro-computed tomography analysis. Immunofluorescence staining was used to investigate the presence of osteocalcin-positive osteoblasts; tartrate-resistant acid phosphatase (TRAP) staining was used to observe osteoclast activity in alveolar bone. Results The level of G-CSF in serum was significantly elevated in mice with periodontitis. Immunofluorescence analyses showed that G-CSF was mostly expressed in the cell membrane of gingival epithelial cells; this expression was enhanced in the periodontitis group. Additionally, systemic administration of anti-G-CSF antibody significantly inhibited alveolar bone resorption, as evidenced by improvements in bone volume/total volume, bone surface area/bone volume, trabecular thickness, trabecular spacing, and trabecular pattern factor values. Immunofluorescence analysis revealed an enhanced number of osteocalcin-positive osteoblasts, while TRAP staining revealed reduction of osteoclast activity. Conclusions G-CSF expression levels were significantly up-regulated in the serum and gingival epithelial cells. Together, anti-G-CSF antibody administration could alleviates alveolar bone resorption, suggesting that G-CSF may be one of the essential immune factors that mediate the bone loss in periodontitis.

scholarly journals Activated STAT3 signaling pathway by ligature-induced periodontitis could contribute to neuroinflammation and cognitive impairment in rats

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yi Hu ◽  
Xu Zhang ◽  
Jing Zhang ◽  
Xinyi Xia ◽  
Huxiao Li ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Locomotor Activity ◽  
Bone Resorption ◽  
Signaling Pathway ◽  
Alveolar Bone ◽  
Periodontal Tissue ◽  
Rt Pcr ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Abstract Background Increasing evidence suggests a causal link between periodontitis and cognitive disorders. Systemic inflammation initiated by periodontitis may mediate the development of cognitive impairment. Our study aims to investigate the effect of ligature-induced periodontitis on cognitive function and the role of signal transducers and activators of transcription 3 (STAT3) in this process. Materials and methods Ligature-induced periodontitis was established, and the rats were treated intraperitoneally with/without the pSTAT3 inhibitor cryptotanshinone (CTS). Alveolar bone resorption and periodontal inflammation were detected by micro-computed tomography analysis and histopathological evaluation. Locomotor activity and cognitive function were evaluated by the open field test and the Morris water maze test, respectively. The activation of microglia and astrocytes in the hippocampus and cortex was assessed by immunohistochemistry (IHC). The expression of interleukins (IL-1β, IL-6, IL-8, IL-21) in both the periphery and cortex was evaluated by RT-PCR and ELISA. The expression of TLR/NF-κB and ROS cascades was evaluated by RT-PCR. The expression of pSTAT3 and the activation of the STAT3 signaling pathway (JAK2, STAT3, and pSTAT3) in the periodontal tissue and cortex were assessed by IHC and Western blot. The expression of amyloid precursor protein (APP) and its key secretases was evaluated by RT-PCR. The level of amyloid β-protein (Aβ) and the ratio of Aβ1-40/1-42 were measured via ELISA in the plasma and cortex while IHC was used to detect the level of Aβ1-42 in the brain. Results In periodontal ligature rats, significant alveolar bone resorption and local inflammatory cell infiltration were present. Apparent increases in inflammatory cytokines (IL-1β, IL-6, IL-8, and IL-21) were detected in peripherial blood and brain. Additionally, spatial learning and memory ability was impaired, while locomotor activity was not affected. Activated microglia and astrocytes were found in the cortex and hippocampus, presenting as enlarged cell bodies and irregular protrusions. Levels of TLR/NF-kB, PPAR and ROS were altered. The STAT3 signaling pathway was activated in both the periodontal tissue and cortex, and the processing of APP by β- and γ-secretases was promoted. The changes mentioned above could be relieved by the pSTAT3 inhibitor CTS. Conclusions Ligature-induced periodontitis in rats resulted in systemic inflammation and further abnormal APP processing, leading to cognitive impairments. In this progress, the activation of the STAT3 signaling pathway may play an important role by increasing inflammatory load and promoting neuroinflammation.

Febuxostat Attenuates the Progression of Periodontitis in Rats

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Naseratun Nessa ◽  
Miyuki Kobara ◽  
Hiroe Toba ◽  
Tetsuya Adachi ◽  
Toshiro Yamamoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Bone Resorption ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Gingival Tissue ◽  
Systemic Effects ◽  
Rt Pcr ◽  
Tnf Α ◽  
And Oxidative Stress

Introduction: Periodontitis is a lifestyle-related disease that is characterized by chronic inflammation in gingival tissue. Febuxostat, a xanthine oxidase inhibitor, exerts anti-inflammatory and antioxidant effects. Objective: The present study investigated the effects of febuxostat on periodontitis in a rat model. Methods: Male Wistar rats were divided into 3 groups: control, periodontitis, and febuxostat-treated periodontitis groups. Periodontitis was induced by placing a ligature wire around the 2nd maxillary molar and the administration of febuxostat (5 mg/kg/day) was then initiated. After 4 weeks, alveolar bone loss was assessed by micro-computed tomography and methylene blue staining. The expression of osteoprotegerin (OPG), a bone resorption inhibitor, was detected by quantitative RT-PCR and immunological staining, and the number of osteoclasts in gingival tissue was assessed by tartrate-resistant acid phosphatase staining. The mRNA and protein expression levels of the proinflammatory cytokines, tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β), in gingival tissue were measured using quantitative RT-PCR and immunological staining. Oxidative stress in gingival tissue was evaluated by the expression of 4-hydroxy-2-nonenal (4-HNE), and 8-hydroxy-2-deoxyguanosine (8-OHdG). To clarify the systemic effects of periodontitis, blood pressure and glucose tolerance were examined. Results: In rats with periodontitis, alveolar bone resorption was associated with reductions in OPG and increases in osteoclast numbers. The gingival expression of TNF-α, IL-1β, 4-HNE, and 8-OHdG was up-regulated in rats with periodontitis. Febuxostat significantly reduced alveolar bone loss, proinflammatory cytokine levels, and oxidative stress. It also attenuated periodontitis-induced glucose intolerance and blood pressure elevations. Conclusion: Febuxostat prevented the progression of periodontitis and associated systemic effects by inhibiting proinflammatory mediators and oxidative stress.

Cerium oxide nanozyme attenuates periodontal bone destruction by inhibiting ROS-NFκB pathway

Nanoscale ◽  
2022 ◽  
Author(s):  
Yijun Yu ◽  
Sheng Zhao ◽  
Deao Gu ◽  
Bijun Zhu ◽  
Hanxiao Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Bone Resorption ◽  
Inflammatory Disease ◽  
Tissue Damage ◽  
Alveolar Bone ◽  
Bone Destruction ◽  
Oxygen Species ◽  
Nfκb Pathway ◽  
Excess Reactive Oxygen Species

Periodontitis, an inflammatory disease of oxidative stress, occurs due to the excess reactive oxygen species (ROS) contributing to cell and tissue damage that in turn leads to alveolar bone resorption...

Tooth Eruption into the Newly Generated Bone Induced by Recombinant Human Bone Morphogenetic Protein-2

2002 ◽  
Vol 39 (4) ◽  
pp. 449-456 ◽  
Author(s):  
Atsushi Kitamura ◽  
Nobuyoshi Motohashi ◽  
Tatsuo Kawamoto ◽  
Yoshiyuki Baba ◽  
Shoichi Suzuki ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Alveolar Bone ◽  
Treated Group ◽  
Tooth Eruption ◽  
Human Bone ◽  
Bone Morphogenetic Protein 2 ◽  
Mineral Density ◽  
Morphogenetic Protein ◽  
Human Bone Morphogenetic Protein ◽  
Recombinant Human Bone

Objective The purpose of this study was to observe tooth eruption pattern into the newly generated bone induced by recombinant human bone morphogenetic protein-2 (rhBMP-2). Method Three 12-week-old beagle dogs were used. Following wound healing of the extracted maxillary third deciduous incisor at the age of 13 weeks, a resection of maxillary alveolar bone (8 mm by 8 mm by 8 mm) was carried out, accompanied by extraction of the maxillary second incisor tooth germ. The rhBMP-2 (5 μg/100 μL or 10 μg/100 μL) was implanted in the resected area. A group that was not implanted after resection and a nonresected group were used as controls. Serial changes of the eruption pattern of the maxillary third incisor in the implanted area were observed radiographically. Oxytetracycline and calcein were employed as bone markers. Nine weeks after the implantation, the animals were sacrificed. The samples were observed histologically and analyzed using peripheral quantitative computerized tomography to acquire the bone mineral density (BMD). Results In the rhBMP-2 (5 μg/100 μL)-treated group, histological findings and the BMD of the newly generated bone were almost same as in the non-resected group. The maxillary third incisor erupted through the implanted area. However, in the rhBMP-2 (10 μg/100 μL)-treated group, more osteoinductive activity and significantly higher BMD were observed in the newly generated bone. The maxillary third incisor erupted mesially so as to avoid this implanted area. Conclusion Results showed that bone remodeling and tooth eruption through the newly generated bone appear to be dose dependent. Accordingly, proper dosage of rhBMP-2 should be determined for successful clinical application.

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