scholarly journals Relationships between tooth eruption, occlusion and alveolar bone resorption: Histochemical and cytological studies of bone remodeling on rat incisor alveolar bone facing the enamel after root resection.

1990 ◽  
Vol 53 (5) ◽  
pp. 511-522 ◽  
Author(s):  
Kazuharu IRIE ◽  
Hidehiro OZAWA
Keyword(s):  
Bone Resorption ◽  
Bone Remodeling ◽  
Alveolar Bone ◽  
Tooth Eruption ◽  
Rat Incisor

scholarly journals Bone Resorption Rate of Moved and Fixed Teeth during Alveolar Bone Remodeling by Orthodontic Treatment.

1998 ◽  
Vol 64 (626) ◽  
pp. 3888-3893
Author(s):  
Hajime MORIKAWA ◽  
Seiki YAMANAMI ◽  
Morimasa NISHIHIRA ◽  
Katsuyuki YAMAMOTO ◽  
Yoshiaki SATOH ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Remodeling ◽  
Orthodontic Treatment ◽  
Alveolar Bone ◽  
Resorption Rate ◽  
Alveolar Bone Remodeling ◽  
Bone Resorption Rate

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.

Role of PTH1R Signaling in Prx1+ Mesenchymal Progenitors during Eruption

2020 ◽  
Vol 99 (11) ◽  
pp. 1296-1305
Author(s):  
C. Cui ◽  
R. Bi ◽  
W. Liu ◽  
S. Guan ◽  
P. Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Bone Remodeling ◽  
Periodontal Ligament ◽  
Alveolar Bone ◽  
Tooth Eruption ◽  
Mesenchymal Progenitors

Tooth eruption is a complex process requiring precise interaction between teeth and adjacent tissues. Molecular analysis demonstrates that bone remodeling plays an essential role during eruption, suggesting that a parathyroid hormone 1 receptor (PTH1R) gene mutation is associated with disturbances in bone remodeling and results in primary failure of eruption (PFE). Recent research reveals the function of PTH1R signaling in mesenchymal progenitors, whereas the function of PTH1R in mesenchymal stem cells during tooth eruption remains incompletely understood. We investigated the specific role of PTH1R in Prx1+ progenitor expression during eruption. We found that Prx1+-progenitors occur in mesenchymal stem cells residing in alveolar bone marrow surrounding incisors, at the base of molars and in the dental follicle and pulp of incisors. Mice with conditional deletion of PTH1R using the Prx1 promoter exhibited arrested mandibular incisor eruption and delayed molar eruption. Micro–computed tomography, histomorphometry, and molecular analyses revealed that mutant mice had significantly reduced alveolar bone formation concomitant with downregulated gene expression of key regulators of osteogenesis in PTH1R-deficient cells. Moreover, culturing orofacial bone-marrow-derived mesenchymal stem cells (OMSCs) from Prx1Cre;PTH1Rfl/fl mice or from transfecting Cre recombinase adenovirus in OMSCs from PTH1Rfl/fl mice suggested that lack of Pth1r expression inhibited osteogenic differentiation in vitro. However, bone resorption was not affected by PTH1R ablation, indicating the observed reduced alveolar bone volume was mainly due to impaired bone formation. Furthermore, we found irregular periodontal ligaments and reduced Periostin expression in mutant incisors, implying loss of PTH1R results in aberrant differentiation of periodontal ligament cells. Collectively, these data suggest that PTH1R signaling in Prx1+ progenitors plays a critical role in alveolar bone formation and periodontal ligament development during eruption. These findings have implications for our understanding of the physiologic and pathologic function of PTH1R signaling in tooth eruption and the progression of PFE.

scholarly journals Evaluation of Bone Resorption Rate during Alveolar Bone Remodeling by Orthodontic Treatment.

1995 ◽  
Vol 61 (589) ◽  
pp. 3545-3551
Author(s):  
Hajime Morikawa ◽  
Morimasa Nishihira ◽  
Katsuyuki Yamamoto ◽  
Hiroyuki Ishikawa ◽  
Yoshiaki Satoh ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Remodeling ◽  
Orthodontic Treatment ◽  
Alveolar Bone ◽  
Resorption Rate ◽  
Alveolar Bone Remodeling ◽  
Bone Resorption Rate

Role of Osteocyte-PDL Crosstalk in Tooth Movement via SOST/Sclerostin

2018 ◽  
Vol 97 (12) ◽  
pp. 1374-1382 ◽  
Author(s):  
N. Odagaki ◽  
Y. Ishihara ◽  
Z. Wang ◽  
E. Ei Hsu Hlaing ◽  
M. Nakamura ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Remodeling ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Control Level ◽  
Compressive Force ◽  
Mechanical Stimuli ◽  
Independent Manner ◽  
Alveolar Bone Remodeling

Sclerostin (Scl) negatively regulates bone formation and favors bone resorption. Osteocytes, the cells responsible for mechanosensing, are known as the primary source of Scl and are a key regulator of bone remodeling through the induction of receptor activator of NF-κB ligand (RANKL). However, the spatiotemporal patterns of Scl in response to mechanical stimuli and their regulatory mechanisms remain unknown. We investigated the regulatory dynamics of the SOST/Scl expression generated by orthodontic tooth movement (OTM) in vivo and in vitro. In 8-wk-old male mice, coil springs were used to move the first molar mesially for 0, 1, 5, or 10 d. A regional histogram and the distribution patterns of the Scl expression showed that the Scl expression in the alveolar bone was increased on the compression side and peaked on day 5, with a gradual increase in the degree of significance. On day 10, the expression around the periodontal ligament (PDL)–alveolar bone boundary returned to the control level. Conversely, the expression of Scl on the tension side was only significantly decreased on day 1. Compressive force biphasically modulated the SOST/Scl expression in the isolated human PDL and thereby upregulated osteocytic SOST via paracrine activation in an osteocyte-PDL co-culture system designed to mimic OTM. This system did not affect the RANKL or OPG expression in osteocytes, suggesting that the bone resorption pathways are acted upon in a PDL-dependent and osteocyte-independent manner through RANKL/OPG signaling. Moreover, sclerostin neutralizing antibody significantly attenuated the upregulation of SOST that was induced by compressive force. In conclusion, our results provide evidence to support that factors secreted by the PDL, including SOST/Scl, control alveolar bone remodeling through osteocytic SOST/Scl in OTM.

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.

scholarly journals Immunolocalization of CSF-1, RANKL and OPG in the enamel-related periodontium of the rat incisor and their implications for alveolar bone remodeling

2009 ◽  
Vol 54 (7) ◽  
pp. 651-657 ◽  
Author(s):  
J.S. Neves ◽  
C.R. Salmon ◽  
N.F. Omar ◽  
E.A.O. Narvaes ◽  
J.R. Gomes ◽  
...  
Keyword(s):  
Bone Remodeling ◽  
Alveolar Bone ◽  
Rat Incisor ◽  
Alveolar Bone Remodeling

scholarly journals Hexavalent chromium exposure alters bone remodeling in the developing tooth alveolus and delays tooth eruption

2021 ◽  
Vol 34 (2) ◽  
pp. 91-97
Author(s):  
Luciana Sánchez ◽  
Ángela Ubios
Keyword(s):  
Bone Resorption ◽  
Bone Remodeling ◽  
Saline Solution ◽  
Potassium Dichromate ◽  
Tooth Eruption ◽  
Control Group ◽  
Equal Dose ◽  
Chromium Exposure ◽  
Experimental Group ◽  
Lower Molar

Although it has been demonstrated that exposure of lactating rats to CrVI delays tooth eruption, the effects of CrVI exposure on bone remodeling in the developing alveolus during tooth eruption remain unknown. Our purpose was to analyze the effect of CrVI in the alveolus of the first lower molar of rats. Thirty-two suckling Wistar rats were divided into two groups. The experimental group received 12.5 mg/kg body weight/day of potassium dichromate dissolved in saline solution by oral gavage as of day 4 of the experiment; the control group received an equal dose of saline solution. Each group was divided into two sub-sets and euthanized at the ages of 9 and 15 days, respectively. Histochemical and histomorphometric studies of the bone surfaces of the developing tooth alveolus were performed. The percentage of bone formation surfaces was lower in experimental animals than in age-matched controls. The percentage of bone resorption surfaces was significantly lower in 9-day-old experimental rats than in controls and significantly higher in 15-day-old experimental rats than in controls. Exposure to CrVI during lactation alters the sequence of bone resorption and formation in the walls of the developing alveolus, both of which are necessary for tooth eruption, thus causing a delay.

scholarly journals Bone Resorption Rate of Moved and Fixed Teeth during Alveolar Bone Remodeling by Orthodontic Treatment.

1999 ◽  
Vol 42 (3) ◽  
pp. 590-596
Author(s):  
Hajime MORIKAWA ◽  
Seiki YAMANAMI ◽  
Morimasa NISHIHIRA ◽  
Katsuyuki YAMAMOTO ◽  
Yoshiaki SATOH ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Remodeling ◽  
Orthodontic Treatment ◽  
Alveolar Bone ◽  
Resorption Rate ◽  
Alveolar Bone Remodeling ◽  
Bone Resorption Rate
Sign in / Sign up

Export Citation Format

Share Document