scholarly journals Parathyroid hormone increases alveolar bone homoeostasis during orthodontic tooth movement in rats with periodontitis via crosstalk between STAT3 and β-catenin

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Cheng Zhang ◽  
Tiancheng Li ◽  
Chenchen Zhou ◽  
Li Huang ◽  
Yuyu Li ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Underlying Mechanism ◽  
Osteoblastic Differentiation ◽  
Alveolar Bone Loss ◽  
Dependent Manner ◽  
Transcription 3

AbstractPeriodontitis patients are at risk of alveolar bone loss during orthodontic treatment. The aim of this study was to investigate whether intermittent parathyroid hormone (1–34) treatment (iPTH) could reduce alveolar bone loss during orthodontic tooth movement (OTM) in individuals with periodontitis and the underlying mechanism. A rat model of OTM in the context of periodontitis was established and alveolar bone loss was observed. The control, iPTH and iPTH + stattic groups received injections of vehicle, PTH and vehicle, or PTH and the signal transducer and activator of transcription 3 (STAT3) inhibitor stattic, respectively. iPTH prevented alveolar bone loss by enhancing osteogenesis and suppressing bone resorption in the alveolar bone during OTM in rats with periodontitis. This effect of iPTH was along with STAT3 activation and reduced by a local injection of stattic. iPTH promoted osteoblastic differentiation and might further regulate the Wnt/β-catenin pathway in a STAT3-dependent manner. The findings of this study suggest that iPTH might reduce alveolar bone loss during OTM in rats with periodontitis through STAT3/β-catenin crosstalk.

Alveolar bone loss induced by the orthodontic tooth movement under hypofunctional conditions in rats

2013 ◽  
Vol 72 (4) ◽  
pp. 148-155 ◽  
Author(s):  
Chisa Shitano ◽  
Otto Baba ◽  
Sawa Kaneko ◽  
Jun Hosomichi ◽  
Yasuhiro Shimizu ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Alveolar Bone Loss

scholarly journals Accelerated tooth movement in Rsk2-deficient mice with impaired cementum formation

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Cita Nottmeier ◽  
Maximilian G. Decker ◽  
Julia Luther ◽  
Simon von Kroge ◽  
Bärbel Kahl-Nieke ◽  
...  
Keyword(s):  
Side Effects ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Alveolar Bone Loss ◽  
Loss Of Function ◽  
Micro Computed Tomography ◽  
Ribosomal S6 Kinase ◽  
Deficient Mice

AbstractCoffin–Lowry–Syndrome (CLS) is a X-linked mental retardation characterized by skeletal dysplasia and premature tooth loss. We and others have previously demonstrated that the ribosomal S6 kinase RSK2, mutated in CLS, is essential for bone and cementum formation; however, it remains to be established whether RSK2 plays also a role in mechanically induced bone remodeling during orthodontic tooth movement (OTM). We, therefore, performed OTM in wild-type (WT) mice and Rsk2-deficient mice using Nitinol tension springs that were fixed between the upper left molars and the incisors. The untreated contralateral molars served as internal controls. After 12 days of OTM, the jaws were removed and examined by micro-computed tomography (µCT), decalcified histology, and immunohistochemistry. Our analysis of the untreated teeth confirmed that the periodontal phenotype of Rsk2-deficient mice is characterized by alveolar bone loss and hypoplasia of root cementum. Quantification of OTM using µCT revealed that OTM was more than two-fold faster in Rsk2-deficient mice as compared to WT. We also observed that OTM caused alveolar bone loss and root resorptions in WT and Rsk2-deficient mice. However, quantification of these orthodontic side effects revealed no differences between WT and Rsk2-deficient mice. Taken together, Rsk2 loss-of-function accelerates OTM in mice without causing more side effects.

scholarly journals Inflammasomes in Alveolar Bone Loss

2021 ◽  
Vol 12 ◽  
Author(s):  
Yang Li ◽  
Junqi Ling ◽  
Qianzhou Jiang
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Remodeling ◽  
Host Defense ◽  
Alveolar Bone ◽  
Bone Destruction ◽  
Alveolar Bone Loss ◽  
Fine Tuning ◽  
Inflammasome Activation ◽  
Dependent Manner

Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast–osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

Implantable zoledronate-PLGA microcapsules ameliorate alveolar bone loss, gingival inflammation and oxidative stress in an experimental periodontitis rat model

2020 ◽  
Vol 35 (6) ◽  
pp. 569-578
Author(s):  
Chun Yao ◽  
Qingqing Zhang ◽  
Jun Li ◽  
Peng She ◽  
Fanzhi Kong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Loss ◽  
Rat Model ◽  
Inflammatory Cytokine ◽  
Alveolar Bone ◽  
Underlying Mechanism ◽  
Alveolar Bone Loss ◽  
Gingival Inflammation ◽  
Cytokine Levels ◽  
And Oxidative Stress

The effect of implantable Zoledronate-PLGA microcapsules (PLGA-ZOL) in periodontitis remains unclear. In this study, we aimed to explore the potential role of PLGA-ZOL in protecting periodontitis and elucidate the underlying mechanism. A rat model of periodontitis was established by ligation the mandibular first molars, then PLGA-ZOL was implanted. The healing volume was scanned by cone-beam computed tomography. Cytokine levels in the gingival tissues were determined by ELISA and RT-PCR. Oxidative stress was indicated by detecting superoxide dismutase concentration and catalase activity. After periodontitis model was successfully established in rats, PLGA-ZOL treatment significantly attenuated alveolar bone loss, as indicated by the increased total healing volume, bone volume/tissue volume and osteoprotegerin level, as well as decreased sRANKL level. PLGA-ZOL treatment also suppressed the inflammatory activities by inhibiting pro-inflammatory cytokine production (TNF-α, IL-1β) but increasing anti-inflammatory cytokine secretion (IL-10). Furthermore, PLGA-ZOL was found to ameliorate oxidative stress in gingival tissues. In conclusion, PLGA-ZOL microcapsules ameliorate alveolar bone loss, gingival inflammation and oxidative stress in an experimental rat model of periodontitis.

Alveolar bone loss in liver transplantation patients: relationship with prolonged steroid treatment and parathyroid hormone levels

2007 ◽  
Vol 34 (12) ◽  
pp. 1039-1045 ◽  
Author(s):  
Orit Oettinger-Barak ◽  
Elena Segal ◽  
Eli E. Machtei ◽  
Shlomi Barak ◽  
Yaacov Baruch ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Parathyroid Hormone ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Steroid Treatment ◽  
Hormone Levels

scholarly journals Distinguish fatty acids impact survival, differentiation and cellular function of periodontal ligament fibroblasts

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Judit Symmank ◽  
Martin Chorus ◽  
Sophie Appel ◽  
Jana Marciniak ◽  
Isabel Knaup ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Periodontal Ligament ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Serum Levels ◽  
Osteoblastic Differentiation ◽  
Mechanical Stimuli ◽  
Periodontal Ligament Fibroblasts

Abstract Alveolar bone (AB) remodeling is necessary for the adaption to mechanical stimuli occurring during mastication and orthodontic tooth movement (OTM). Thereby, bone degradation and assembly are strongly regulated processes that can be altered in obese patients. Further, increased fatty acids (FA) serum levels affect bone remodeling cells and we, therefore, investigated whether they also influence the function of periodontal ligament fibroblast (PdLF). PdLF are a major cell type regulating the differentiation and function of osteoblasts and osteoclasts localized in the AB. We stimulated human PdLF (HPdLF) in vitro with palmitic (PA) or oleic acid (OA) and analyzed their metabolic activity, growth, survival and expression of osteogenic markers and calcium deposits. Our results emphasize that PA increased cell death of HPdLF, whereas OA induced their osteoblastic differentiation. Moreover, quantitative expression analysis of OPG and RANKL revealed altered levels in mechanically stimulated PA-treated HPdLF. Furthermore, osteoclasts stimulated with culture medium of mechanical stressed FA-treated HPdLF revealed significant changes in cell differentiation upon FA-treatment. For the first time, our results highlight a potential role of specific FA in the function of HPdLF-modulated AB remodeling and help to elucidate the complex interplay of bone metabolism, mechanical stimulation and obesity-induced alterations.

Phytocystatin CsinCPI-2 Reduces Osteoclastogenesis and Alveolar Bone Loss

2021 ◽  
pp. 002203452110278
Author(s):  
N. Da Ponte Leguizamón ◽  
R.S. de Molon ◽  
G. Coletto-Nunes ◽  
A.V.B. Nogueira ◽  
S.V. Rocha ◽  
...  
Keyword(s):  
Bone Loss ◽  
Connective Tissue ◽  
Alveolar Bone ◽  
Osteoclast Differentiation ◽  
Alveolar Bone Loss ◽  
Inflammatory Cell Infiltrate ◽  
Mouse Bone Marrow ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Chronic Inflammatory Condition

Periodontal disease (PD) is a polymicrobial chronic inflammatory condition of the supporting tissues around the teeth, leading to the destruction of surrounding connective tissue. During the progression of PD, osteoclasts play a crucial role in the resorption of alveolar bone that eventually leads to the loss of teeth if the PD is left untreated. Therefore, the development of antiresorptive therapies targeting bone-resorbing cells will significantly benefit the treatment of PD. Here, we demonstrate the inhibitory effect of CsinCPI-2, a novel cysteine peptidase inhibitor from the orange tree, on periodontitis-induced inflammation, alveolar bone loss, and osteoclast differentiation. Using the ligature-induced periodontitis model in mice, we show that treatment with CsinCPI-2 (0.8 µg/g of body weight) significantly reduced inflammatory cell infiltrate in the connective tissue and prevented the loss of alveolar bone mass (BV/TV) caused by PD, effects associated with diminished numbers of TRAP-positive multinucleated cells. Furthermore, CsinCPI-2 significantly downregulated the numbers of inflammatory cells expressing CD3, CD45, MAC387, and IL-1β. In vitro, CsinCPI-2 inhibited RANKL-induced TRAP+ multinucleated osteoclast formation in mouse bone marrow macrophage cultures in a concentration-dependent manner. This effect was not due to cytotoxicity, as demonstrated by the MTT assay. CsinCPI-2 inhibited RANKL-induced mRNA expression of Acp5, Calcr, and Ctsk, as well as the RANKL-induced upregulation of Nfatc1, a crucial transcription factor for osteoclast differentiation. Based on our findings, CsinCPI-2 prevents bone loss induced by PD by controlling the inflammatory process and acting directly on osteoclastogenesis, suggesting an interesting potential for CsinCPI-2 in the strategy for PD treatment.

Sign in / Sign up

Export Citation Format

Share Document