scholarly journals Association between Postmenopausal Osteoporosis and Experimental Periodontitis

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Kai Luo ◽  
Souzhi Ma ◽  
Jianbin Guo ◽  
Yongling Huang ◽  
Fuhua Yan ◽  
...  
Keyword(s):  
Postmenopausal Osteoporosis ◽  
Alveolar Bone ◽  
Ovariectomized Rats ◽  
Whole Body ◽  
Inflammatory Factors ◽  
Mineral Density ◽  
Metabolic Markers ◽  
Periodontal Tissues ◽  
Experimental Periodontitis ◽  
Turnover Markers

To investigate the correlation between postmenopausal osteoporosis (PMO) and the pathogenesis of periodontitis, ovariectomized rats were generated and the experimental periodontitis was induced using a silk ligature. The inflammatory factors and bone metabolic markers were measured in the serum and periodontal tissues of ovariectomized rats using an automatic chemistry analyzer, enzyme-linked immunosorbent assays, and immunohistochemistry. The bone mineral density of whole body, pelvis, and spine was analyzed using dual-energy X-ray absorptiometry and image analysis. All data were analyzed using SPSS 13.0 statistical software. It was found that ovariectomy could upregulate the expression of interleukin- (IL-)6, the receptor activator of nuclear factor-κB ligand (RANKL), and osteoprotegerin (OPG) and downregulate IL-10 expression in periodontal tissues, which resulted in progressive alveolar bone loss in experimental periodontitis. This study indicates that changes of cytokines and bone turnover markers in the periodontal tissues of ovariectomized rats contribute to the damage of periodontal tissues.

scholarly journals Extracellular regulated kinase 5 mediates osteoporosis through modulating viability and apoptosis of osteoblasts in ovariectomized rats

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Tuan-Mao Guo ◽  
Yan-Li Xing ◽  
Hai-Yun Zhu ◽  
Lan Yang ◽  
Guo-Xiong Liu ◽  
...  
Keyword(s):  
Bone Turnover ◽  
Postmenopausal Osteoporosis ◽  
Biomechanical Properties ◽  
Ovariectomized Rats ◽  
Sprague Dawley ◽  
Mineral Density ◽  
Alp Activity ◽  
Extracellular Signal ◽  
Osteoblast Apoptosis ◽  
Turnover Markers

Abstract Postmenopausal osteoporosis is a common condition characterized by the increase and activation of osteoclasts. The present study aimed to investigate the effects of extracellular signal-regulated kinase (ERK) 5 (ERK-5) on postmenopausal osteoporosis by regulating the biological behaviors of osteoblasts. Sprague–Dawley (SD) rats were ovariectomized to develop an osteoporosis model. A lentivirus packaging system was employed to generate lentiviruses capable of up- or down-regulating the expression of ERK-5 in ovariectomized rats. The femoral biomechanical properties, bone mineral density (BMD), contents of calcium (Ca), phosphorus (P) and alkaline phosphatase (ALP) and bone turnover markers in rats, as well as viability, cycle and apoptosis of osteoblasts and ALP activity in osteoblasts were measured in the ovariectomized rats so as to explore the functional significance of ERK-5 in postmenopausal osteoporosis. The femoral mechanical strength of ovariectomized rats was enhanced by overexpression of ERK-5. Meanwhile femoral BMD, and bone metabolism were increased, and bone turnover normalized in the ovariectomized rats when ERK-5 was overexpressed. Lentivirus-mediated ERK-5 overexpression in osteoblasts was observed to inhibit osteoblast apoptosis, and promote viability, accompanied with increased ALP activity. Taken together, ERK-5 could decelerate osteoblast apoptosis and improve postmenopausal osteoporosis by increasing osteoblast viability. Thus, our study provides further understanding on a promising therapeutic target for postmenopausal osteoporosis.

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 Effects of the Peroxisome Proliferator-Activated Receptor (PPAR)-δ Agonist GW501516 on Bone and Muscle in Ovariectomized Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (6) ◽  
pp. 2178-2189 ◽  
Author(s):  
M. P. Mosti ◽  
A. K. Stunes ◽  
M. Ericsson ◽  
H. Pullisaar ◽  
J. E. Reseland ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Bone Loss ◽  
Ovariectomized Rats ◽  
Whole Body ◽  
Control Group ◽  
High Dose ◽  
Peroxisome Proliferator ◽  
Mineral Density ◽  
Muscle Morphology ◽  
Ovx Rats

Estrogen deficiency promotes bone loss and skeletal muscle dysfunction. Peroxisome proliferator-activated receptors (PPARs) have 3 subtypes (α, δ, and γ). PPARγ agonists induce bone loss, whereas PPARα agonists increase bone mass. Although PPARδ agonists are known to influence skeletal muscle metabolism, the skeletal effects are unsettled. This study investigated the musculoskeletal effects of the PPARδ agonist GW501516 in ovariectomized (OVX) rats. Female Sprague Dawley rats, 12 weeks of age, were allocated to a sham-operated group and 3 OVX groups; high-dose GW501516 (OVX-GW5), low-dose GW501516 (OVX-GW1), and a control group (OVX-CTR), respectively (n = 12 per group). Animals received GW501516 or vehicle (methylcellulose) daily for 4 months by gavage. Bone mineral density (BMD) was assessed by dual x-ray absorptiometry at the femur, spine, and whole body. Bone microarchitecture at the proximal tibia was assessed by microcomputed tomography, and dynamic histomorphometry was performed. Quadriceps muscle morphology and the relative expression of mitochondrial proteins were analyzed. Bone metabolism markers and metabolic markers were measured in plasma. After 4 months, the OVX-GW5 group displayed lower femoral BMD than OVX-CTR. Trabecular separation was higher in the GW-treated groups, compared with OVX-CTR. The OVX-GW5 group also exhibited lower cortical area fraction and a higher structure model index than OVX-CTR. These effects coincided with impaired bone formation in both GW groups. The OVX-GW5 group displayed elevated triglyceride levels and reduced adiponectin levels, whereas no effects on muscle morphology or mitochondrial gene expression appeared. In summary, the PPARδ agonist GW501516 negatively affected bone properties in OVX rats, whereas no effects were detected in skeletal muscle.

scholarly journals PTEN Inhibits Inflammatory Bone Loss in Ligature-Induced Periodontitis via IL1 and TNF-α

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Chuanyun Fu ◽  
Zhimin Wei ◽  
Dongsheng Zhang
Keyword(s):  
Bone Remodeling ◽  
Alveolar Bone ◽  
Bone Erosion ◽  
Interleukin 1 ◽  
Inflammatory Factors ◽  
Oral Diseases ◽  
Periodontal Tissues ◽  
Tensin Homolog ◽  
Key Factor

Phosphatase and tensin homolog (PTEN) is a critical regulator of tumorigenesis and bone remodeling, which is also found expressed in the periodontal tissues. Periodontitis is one of the most common oral diseases and associated with alveolar bone resorption and tooth loosening in adults. However, the functional relevance of PTEN in periodontitis remains unclear. Here, we report that PTEN plays an essential role in periodontitis. The in vivo results of our study showed a significant decrease of PTEN in the ligature-induced mouse periodontitis model. The function of PTEN in the macrophages was shown to be associated with inflammatory factors interleukin 1 (IL1) and tumor necrosis factor (TNF-α) by using overexpression and silence methods. Further mechanistic studies indicated lack of PTEN-activated IL1 and TNF-α, which increased the number of osteoclasts and led to alveolar bone erosion and loss. Moreover, PTEN nanoparticles could directly inhibit the inflammatory process and bone erosion, suggesting a controlling role of PTEN during bone remodeling. All these data identified the novel function of PTEN as a key factor in periodontitis and bone remodeling.

scholarly journals Serumβ-Catenin Levels Associated with the Ratio of RANKL/OPG in Patients with Postmenopausal Osteoporosis

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Xiao-Juan Xu ◽  
Lin Shen ◽  
Yan-Ping Yang ◽  
Rui Zhu ◽  
Bo Shuai ◽  
...  
Keyword(s):  
Bone Turnover ◽  
Postmenopausal Women ◽  
Postmenopausal Osteoporosis ◽  
Bone Turnover Markers ◽  
Enzyme Linked Immunosorbent Assay ◽  
Functional Communication ◽  
Mineral Density ◽  
Wnt Pathways ◽  
Turnover Markers

Objective. To demonstrate the role of Wnt/β-catenin canonical pathway in postmenopausal osteoporosis by evaluating serumβ-catenin levels in patients with postmenopausal osteoporosis and analyzing their possible relationship with serum OPG, RANKL, the ratio of RANKL/OPG, sclerostin, and bone turnover markers.Methods. 480 patients with postmenopausal osteoporosis and 170 healthy postmenopausal women were enrolled in the study. Serumβ-catenin, OPG, RANKL, and sclerostin levels were measured by enzyme-linked immunosorbent assay. Bone status was assessed by measuring bone mineral density and bone turnover markers. Estradiol levels were also detected.Results. Serumβ-catenin levels were lower in postmenopausal osteoporotic women compared to nonosteoporotic postmenopausal women (26.26±14.81versus39.33±5.47 pg/mL,P<0.001). Serumβ-catenin was positively correlated with osteoprotegerin (r=0.232,P<0.001) and negatively correlated with the ratio of RANKL/OPG, body mass index, and sclerostin (r=-0.128,P=0.005;r=-0.117,P=0.010;r=-0.400,P<0.001, resp.) in patients with postmenopausal osteoporosis.Conclusion. The results indicate that lower serumβ-catenin and concomitantly higher ratio of RANKL/OPG may be involved in the pathogenesis of postmenopausal osteoporosis. Functional communication between RANKL/RANK/OPG system and Wnt pathways plays an important role in postmenopausal osteoporosis.

Involvement of Cot/Tp12 in Bone Loss during Periodontitis

2010 ◽  
Vol 89 (2) ◽  
pp. 192-197 ◽  
Author(s):  
T. Ohnishi ◽  
A. Okamoto ◽  
K. Kakimoto ◽  
K. Bandow ◽  
N. Chiba ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Periodontal Tissue ◽  
Rankl Expression ◽  
Periodontal Tissues ◽  
Tnf Α ◽  
Experimental Periodontitis ◽  
Deficient Mice

Periodontitis causes resorption of alveolar bone, in which RANKL induces osteoclastogenesis. The binding of lipopolysaccharide to Toll-like receptors causes phosphorylation of Cot/Tp12 to activate the MAPK cascade. Previous in vitro studies showed that Cot/Tp12 was essential for the induction of RANKL expression by lipopolysaccharide. In this study, we examined whether Cot/Tp12 deficiency reduced the progression of alveolar bone loss and osteoclastogenesis during experimental periodontitis. We found that the extent of alveolar bone loss and osteoclastogenesis induced by ligature-induced periodontitis was decreased in Cot/Tp12-deficient mice. In addition, reduction of RANKL expression was observed in periodontal tissues of Cot/Tp12-deficient mice with experimental periodontitis. Furthermore, we found that Cot/Tp12 was involved in the induction of TNF-α mRNA expression in gingiva of mice with experimental periodontitis. Our observations suggested that Cot/Tp12 is essential for the progression of alveolar bone loss and osteoclastogenesis in periodontal tissue during experimental periodontitis mediated through increased RANKL expression.

scholarly journals Protective Effect of Resveratrol against the Alveolar Bone Loss in Rats with Experimental Periodontitis and Acts Positively on the IL-17

2021 ◽  
pp. 162-173
Author(s):  
JordanaHeidemann Pandini ◽  
Lais Fernanda Pasqualotto ◽  
Pedro Henrique de Carli Rodrigues ◽  
João Paulo Gonçalves De Paivaa ◽  
Patricia Oehlmeyer Nassar ◽  
...  
Keyword(s):  
Bone Loss ◽  
Protective Effect ◽  
Alveolar Bone ◽  
Experimental Period ◽  
Alveolar Bone Loss ◽  
Control Group ◽  
Interleukin 17 ◽  
Periodontal Tissues ◽  
Male Wistar Rats ◽  
Experimental Periodontitis

The resveratrol is a polyphenol known for its health benefits, which includes the ability to interfere in the osteoblastogenesis, which may foster adverse immunomodulators effects in the host response to periodontal disease. In the present study we evaluated the appearance of periodontal tissues of rats with experimentally induced periodontitis, by using resveratrol. Twenty-four male Wistar rats were used, in which half of the animals received a ligature around the first lower molars, then forming the groups with experimental periodontitis. Next, four groups were created: 1) Control Group (CON); 2) The Ligature Group (LIG); 3) Group Resveratrol (RSV); 4) Ligature-Resveratrol Group (LIG-RSV). The animals of the Resveratrol groups were daily dosed with 10 mg/kg of body weight of polyphenol orally, during four weeks. After 105 days of experimental period, euthanasia was performed. The results showed a significantly lower alveolar bone loss (p<0.05) in animals that received resveratrol, and still, the polyphenol was able to reduce concentration of interleukin 17 (IL-17) in the groups dosed with it. Our conclusion is that dosing rats with experimental periodontitis with resveratrol could cause a protective effect on the alveolar bone loss, in addition to act positively on the IL-17.

scholarly journals Antiresorptive Therapy and the Bone Turnover Markers—Assessed Fracture Risk in Postmenopausal Women

2020 ◽  
Author(s):  
Ljiljana Smilic ◽  
Tanja Smilic ◽  
Aleksandar N. Jovanovic ◽  
Snezana R. Markovic - Jovanovic ◽  
Zlatica Mirkovic ◽  
...  
Keyword(s):  
Bone Turnover ◽  
Fracture Risk ◽  
Postmenopausal Women ◽  
Bone Turnover Markers ◽  
Bone Markers ◽  
Antiresorptive Therapy ◽  
Mineral Density ◽  
Metabolic Markers ◽  
Increased Risk ◽  
Turnover Markers

Abstract Purpose/Introduction: The aim of this study was to determine relationship of the bone markers levels with the fracture risk and treatment monitoring in patients with osteoporosis. Bone markers may point out to on specific aspects of bone quality, detecting changes of bone mineral density, thus providing prognostic perspective and accounting for a substantial proportion of fracture risk reduction.Methods: The case-control study comprised data from 55 patients undergoing evaluation for osteoporosis at Medicus Universalis Polyclinic in Krusevac. Densitometric findings, P1NP, CTX and osteocalcin levels were determined in all patients twice – at the first assessment and 6 months after. While 30 patients took no medical therapy, 25 of them were treated with ibandronate. Results: No convincing difference in densitometric measurements between patients with and without prevalent fractures were noted, while mean osteocalcin and P1NP levels were significantly lower (p<0.05) in osteoporotic patients who suffered fractures. A significant correlation between those bone turnover markers and T-score was established, especially in the second measurement and in patients treated with ibandronate.Conclusion: In postmenopausal women and individuals with low BMD, the presence of increased bone turnover markers suggests an increased risk of fractures. Furthermore, these metabolic markers are useful in the monitoring of patients receiving antiresorptive therapy, wherein fast decline of their levels indicate favorable course. Their determination after 6 months offers the remarkable advantage in assessing the effectiveness of medical treatment comparing to 12–24 months required to document changes by BMD.

scholarly journals Influence of the treatment with the antineoplastic agents 5-fluorouracil and Cisplatin on the severity of experimental periodontitis in rats

2021 ◽  
Author(s):  
vivian novaes ◽  
Edilson Ervolino ◽  
Giovani Lopes Fernandes ◽  
Clara Possarle Cunha ◽  
Leticia Helena Theodoro ◽  
...  
Keyword(s):  
Antineoplastic Agents ◽  
Alveolar Bone ◽  
Physiological Saline ◽  
Male Rats ◽  
Lower Percentage ◽  
Periodontal Tissues ◽  
Periodontal Breakdown ◽  
Physiological Saline Solution ◽  
Treatment Data ◽  
Experimental Periodontitis

Abstract Purpose The determination on how antineoplastic agents interfere on the progression of periodontitis is critical for improvement and even development of novel therapeutic approaches for periodontal management. This study evaluated the influence of chemotherapy with 5-fluorouracil (5-FU) or cisplatin (CIS) on healthy periodontal tissues and on the progression of experimental periodontitis (EP). Methods One-hundred-forty-four male rats were divided into six groups (n = 24). Each group was treated with physiological saline solution (PSS) 0.9%, 5-FU or CIS. Experimental periodontitis (EP) was induced by ligature placement. Animals were euthanized at 7, 15 and 30 days after treatment. Data were statistically analyzed (p ≤ 0.05). Results The groups with EP and treated with 5-FU or CIS showed lower percentage of bone volume in the furcation region and higher percentage of alveolar bone loss, higher number of TRAP-positive cells and lower number of PCNA-positive cells when compared group with EP and treated with PSS (p ≤ 0.05). Groups with EP and treated with 5-FU or CIS showed high immunolabelling pattern of RANKL, TNF-α, IL-1β, moderate of BAX and low of HIF-1α. Histological analysis showed severe tissue breakdown in the groups with EP and treated with 5-FU or CIS. Conclusions Chemotherapy with antineoplastic agents 5-FU and CIS increasing the intensity and duration of the inflammation; and compromising tissue repair by reduction in cellular and vascular turnover. The more severe periodontal breakdown was caused by 5-FU.

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