scholarly journals Effects of DSPP Gene Mutations on Periodontal Tissues

2021 ◽  
Author(s):  
Zhaojun Jing ◽  
Zhibin Chen ◽  
Yong Jiang
Keyword(s):  
Alveolar Bone ◽  
Gene Mutations ◽  
Specific Protein ◽  
Dentinogenesis Imperfecta ◽  
Dentin Sialophosphoprotein ◽  
Periodontal Tissues ◽  
Furcation Involvement ◽  
Almost All ◽  
Alveolar Bone Defect ◽  
Deficient Mice

AbstractDentin sialophosphoprotein (DSPP) gene mutations cause autosomal dominantly inherited diseases. DSPP gene mutations lead to abnormal expression of DSPP, resulting in a series of histological, morphological, and clinical abnormalities. A large number of previous studies demonstrated that DSPP is a dentinal-specific protein, and DSPP gene mutations lead to dentin dysplasia and dentinogenesis imperfecta. Recent studies have found that DSPP is also expressed in bone, periodontal tissues, and salivary glands. DSPP is involved in the formation of the periodontium as well as tooth structures. DSPP deficient mice present furcation involvement, cementum, and alveolar bone defect. We speculate that similar periodontal damage may occur in patients with DSPP mutations. This article reviews the effects of DSPP gene mutations on periodontal status. However, almost all of the research is about animal study, there is no evidence that DSPP mutations cause periodontium defects in patients yet. We need to conduct systematic clinical studies on DSPP mutation families in the future to elucidate the effect of DSPP gene on human periodontium.

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.

Orthodontic Force–Induced BMAL1 in PDLCs Is a Vital Osteoclastic Activator

2021 ◽  
pp. 002203452110199
Author(s):  
Y. Xie ◽  
Q. Tang ◽  
S. Yu ◽  
W. Zheng ◽  
G. Chen ◽  
...  
Keyword(s):  
Bone Remodeling ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Nuclear Factor Κb ◽  
Periodontal Ligament Cells ◽  
Orthodontic Force ◽  
Periodontal Tissues ◽  
Alveolar Bone Remodeling ◽  
Biomechanical Stimuli

Orthodontic tooth movement (OTM) depends on periodontal ligament cells (PDLCs) sensing biomechanical stimuli and subsequently releasing signals to initiate alveolar bone remodeling. However, the mechanisms by which PDLCs sense biomechanical stimuli and affect osteoclastic activities are still unclear. This study demonstrates that the core circadian protein aryl hydrocarbon receptor nuclear translocator–like protein 1 (BMAL1) in PDLCs is highly involved in sensing and delivering biomechanical signals. Orthodontic force upregulates BMAL1 expression in periodontal tissues and cultured PDLCs in manners dependent on ERK (extracellular signal–regulated kinase) and AP1 (activator protein 1). Increased BMAL1 expression can enhance secretion of CCL2 (C-C motif chemokine 2) and RANKL (receptor activator of nuclear factor–κB ligand) in PDLCs, which subsequently promotes the recruitment of monocytes that differentiate into osteoclasts. The mechanistic delineation clarifies that AP1 induced by orthodontic force can directly interact with the BMAL1 promoter and activate gene transcription in PDLCs. Localized administration of the ERK phosphorylation inhibitor U0126 or the BMAL1 inhibitor GSK4112 suppressed ERK/AP1/BMAL1 signaling. These treatments dramatically reduced osteoclastic activity in the compression side of a rat orthodontic model, and the OTM rate was almost nonexistent. In summary, our results suggest that force-induced expression of BMAL1 in PDLCs is closely involved in controlling osteoclastic activities during OTM and plays a vital role in alveolar bone remodeling. It could be a useful therapeutic target for accelerating the OTM rate and controlling pathologic bone-remodeling activities.

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 Inflammation in the Human Periodontium Induces Downregulation of the α1- and β1-Subunits of the sGC in Cementoclasts

2021 ◽  
Vol 22 (2) ◽  
pp. 539
Author(s):  
Yüksel Korkmaz ◽  
Behrus Puladi ◽  
Kerstin Galler ◽  
Peer W. Kämmerer ◽  
Agnes Schröder ◽  
...  
Keyword(s):  
Protein Expression ◽  
Alveolar Bone ◽  
Soluble Guanylyl Cyclase ◽  
Cathepsin K ◽  
Staining Intensity ◽  
Cyclic Guanosine Monophosphate ◽  
Heme Iron ◽  
Guanosine Monophosphate ◽  
Independent Manner ◽  
Periodontal Tissues

Nitric oxide (NO) binds to soluble guanylyl cyclase (sGC), activates it in a reduced oxidized heme iron state, and generates cyclic Guanosine Monophosphate (cGMP), which results in vasodilatation and inhibition of osteoclast activity. In inflammation, sGC is oxidized and becomes insensitive to NO. NO- and heme-independent activation of sGC requires protein expression of the α1- and β1-subunits. Inflammation of the periodontium induces the resorption of cementum by cementoclasts and the resorption of the alveolar bone by osteoclasts, which can lead to tooth loss. As the presence of sGC in cementoclasts is unknown, we investigated the α1- and β1-subunits of sGC in cementoclasts of healthy and inflamed human periodontium using double immunostaining for CD68 and cathepsin K and compared the findings with those of osteoclasts from the same sections. In comparison to cementoclasts in the healthy periodontium, cementoclasts under inflammatory conditions showed a decreased staining intensity for both α1- and β1-subunits of sGC, indicating reduced protein expression of these subunits. Therefore, pharmacological activation of sGC in inflamed periodontal tissues in an NO- and heme-independent manner could be considered as a new treatment strategy to inhibit cementum resorption.

scholarly journals Leucocyte- and Platelet-Rich Fibrin Block: Its Use for the Treatment of a Large Cyst with Implant-Based Rehabilitation

Medicina ◽  
2021 ◽  
Vol 57 (2) ◽  
pp. 180 ◽  
Author(s):  
Rodolfo Mauceri ◽  
Denise Murgia ◽  
Orazio Cicero ◽  
Luigi Paternò ◽  
Luca Fiorillo ◽  
...  
Keyword(s):  
Bone Regeneration ◽  
Bone Defect ◽  
Bone Healing ◽  
Bone Substitute ◽  
Alveolar Bone ◽  
Critical Size ◽  
Large Bone ◽  
Alveolar Bone Defect ◽  
Positive Results ◽  
Autologous Platelet

The management of critical-size bone defects is still demanding. Recently, autologous platelet concentrates in combination with bone substitute have been applied and reported in a few studies. Our aim is to report the healing of a critical-size alveolar bone defect treated with a new bone regeneration technique by means of L-PRF and L-PRF blocks. A 45-year-old woman presented a large cystic lesion; the extraction of three teeth, a cyst removal procedure, and bone regeneration procedures with L-PRF and L-PRF blocks were planned. The L-PRF block was prepared by mixing a bone substitute with a piece of L-PRF membrane and liquid fibrinogen. Additionally, after bone healing an implant-based rehabilitation was optimally performed. On the basis of the positive results, in terms of bone healing and tissue regeneration in a large bone defect, the application of L-PRF and L-PRF blocks, in agreement with the scarce literature, is suggested as a feasible procedure in selected cases.

scholarly journals A role for CD9 molecules in T cell activation.

1996 ◽  
Vol 184 (2) ◽  
pp. 753-758 ◽  
Author(s):  
X G Tai ◽  
Y Yashiro ◽  
R Abe ◽  
K Toyooka ◽  
C R Wood ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Immune Responses ◽  
T Cell Activation ◽  
Cell Activation ◽  
Expression Cloning ◽  
Wild Type ◽  
Almost All ◽  
Antigen Presenting ◽  
Deficient Mice

Costimulation mediated by the CD28 molecule plays an important role in optimal activation of T cells. However, CD28-deficient mice can mount effective T cell-dependent immune responses, suggesting the existence of other costimulatory systems. In a search for other costimulatory molecules on T cells, we have developed a monoclonal antibody (mAb) that can costimulate T cells in the absence of antigen-presenting cells (APC). The molecule recognized by this mAb, 9D3, was found to be expressed on almost all mature T cells and to be a protein of approximately 24 kD molecular mass. By expression cloning, this molecule was identified as CD9, 9D3 (anti-CD9) synergized with suboptimal doses of anti-CD3 mAb in inducing proliferation by virgin T cells. Costimulation was induced by independent ligation of CD3 and CD9, suggesting that colocalization of these two molecules is not required for T cell activation. The costimulation by anti-CD9 was as potent as that by anti-CD28. Moreover, anti-CD9 costimulated in a CD28-independent way because anti-CD9 equally costimulated T cells from the CD28-deficient as well as wild-type mice. Thus, these results indicate that CD9 serves as a molecule on T cells that can deliver a potent CD28-independent costimulatory signal.

Compressive Force Induces VEGF Production in Periodontal Tissues

2009 ◽  
Vol 88 (8) ◽  
pp. 752-756 ◽  
Author(s):  
A. Miyagawa ◽  
M. Chiba ◽  
H. Hayashi ◽  
K. Igarashi
Keyword(s):  
Alveolar Bone ◽  
Tooth Movement ◽  
Vascular System ◽  
Orthodontic Tooth Movement ◽  
Compressive Force ◽  
Vegf Mrna ◽  
Angiogenic Activity ◽  
Periodontal Tissues ◽  
Pdl Cells

During orthodontic tooth movement, the activation of the vascular system in the compressed periodontal ligament (PDL) is an indispensable process in tissue remodeling. We hypothesized that compressive force would induce angiogenesis of PDL through the production of vascular endothelial growth factor (VEGF). We examined the localization of VEGF in rat periodontal tissues during experimental tooth movement in vivo, and the effects of continuous compressive force on VEGF production and angiogenic activity in human PDL cells in vitro. PDL cells adjacent to hyalinized tissue and alveolar bone on the compressive side showed marked VEGF immunoreactivity. VEGF mRNA expression and production in PDL cells increased, and conditioned medium stimulated tube formation. These results indicate that continuous compressive force enhances VEGF production and angiogenic activity in PDL cells, which may contribute to periodontal remodeling, including angiogenesis, during orthodontic tooth movement.

scholarly journals Management of Chronic Gingivitis with localized periodontitis by Nonsurgical (Phase I) Periodontal Therapy- A Case Report

2018 ◽  
Vol 7 (2) ◽  
pp. 33-37
Author(s):  
Md Huzzatul Islam Khan ◽  
Sultana Akter Eka ◽  
Md Ashif Iqbal
Keyword(s):  
Phase I ◽  
Oral Hygiene ◽  
Alveolar Bone ◽  
Bone Destruction ◽  
Chronic Inflammatory Disease ◽  
Periodontal Therapy ◽  
Periodontal Treatment ◽  
Periodontal Tissues ◽  
Hygiene Measures ◽  
Tissue Flap

Periodontitis is a chronic inflammatory disease of the periodontal tissues (periodontium) which surround and support the teeth, that results in attachment loss and alveolar bone destruction leads to ultimate tooth loss. It is caused by the bacteria present in dental plaque, which is a tenacious substance that forms on teeth and gingiva just after teeth are brushed. Periodontal treatment is aimed at controlling the infection in order to stop the progression of the disease and to be able to maintain a healthy periodontium. Mechanical debridement of supragingival and subgingival biofilms, together with adequate oral hygiene measures is the standard periodontal therapy. This mechanical subgingi- val biofilm debridement consists of an initial (nonsurgical /phase I) phase involving scaling and root planing (SRP) and the elimination of plaque retentive factors, followed by a surgical phase (if needed) including the elevation of a tissue flap and bone remodeling in further stages. The adjunct use of antibiotics has proven to additionally improve the outcome of periodontal treatment. A clinical case of a 40-years-old male patient with generalized severe chronic periodontitis with localized gingival swell- ing was treated with nonsurgical (phase I) periodontal therapy that was confined to oral hygiene instruction (OHI), SRP with an adjunct antimicrobial regimen.Update Dent. Coll. j: 2017; 7 (2): 33-37

scholarly journals Macroscopic analysis of dental and periodontal tissues of pig (Sus domesticus) exposed to high temperatures

2017 ◽  
Vol 21 (1) ◽  
pp. 28-34
Author(s):  
Sebastián Medina ◽  
Sandra Henao ◽  
Viviana Muñóz ◽  
Carolina López ◽  
Juan Esteban Gutiérrez ◽  
...  
Keyword(s):  
High Temperatures ◽  
Alveolar Bone ◽  
Great Resistance ◽  
Dental Identification ◽  
Color Changes ◽  
Dental Tissues ◽  
Periodontal Tissues ◽  
Sus Domesticus ◽  
Physical Changes ◽  
Macroscopic Analysis

SUMMARYObjective: To describe the physical changesofmacro-structural dental tissues (enamel,dentin and cement) and periodontal(oral mucous membrane, alveolar compactbone and cancellous alveolar bone) ofdomestic pig (Sus domesticus) expose tohigh temperatures.Materials and methods: This descriptivestudy observed the physical changes in macro-structural dental tissues and periodontalin 25 teeth of domestic pigs subjected tohigh temperatures (200°C, 400°C, 600°C,800°C and 1000°C).Results: Dental and periodontal tissues studiedshow great resistance when subjectedto high temperatures without changing significantlytheir macro-structure. At 200°Cno color changes and cracks appear in theenamel. At 400°C there was an increase ofthe fissure and no separation between thehard tissues, initiating carbonization. At600°C fractures in the dental tissues andbone are most apparent. At 800°C burningof the tissues initiated. At 1000°C there wasno evidence of soft tissue.Conclusions: Macroscopic analysis of theteeth articulated in their alveolar-dentalunits constitutes a experimental model thatssimulates the changes of dental and periodontaltissues expose to high temperature.It is recommended to conduct astudy onhuman teeth in their respective unit articulatedalveolar to determine whether themacro-structural physical changes describedare repeated and can be extrapolated,and which can eventually be used duringthe process of dental identification anddocumentation of the medical legal autopsyused in the case of bodies or human remainsburned, charred and burned.Key words: Forensic dentistry, domesticpig (Sus domesticus), dental and periodontaltissues, temperature exposition, animalmodel.

Sign in / Sign up

Export Citation Format

Share Document