scholarly journals The role of probiotic on alveolar bone resorption

2011 ◽  
Vol 44 (3) ◽  
pp. 117
Author(s):  
Desi Sandra Sari ◽  
Zahara Meilawaty ◽  
M. Nurul Amin
2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Carolyn G. J. Moonen ◽  
Teun J. de Vries ◽  
Patrick Rijkschroeff ◽  
Patrice E. Poubelle ◽  
Elena A. Nicu ◽  
...  

The ligand of the receptor activator of NF-κB (RANKL) is a key molecule in the formation of osteoclasts, the key cells that cause the disease-associated alveolar bone resorption in periodontitis. We hypothesized that polymorphonuclear leukocytes (PMNs), found as the most prominent cells of inflamed periodontal tissues, could play an important role in providing signals to trigger osteoclastogenesis and thus activating pathological bone resorption in periodontitis. RANKL expression was investigated on circulatory PMNs (cPMNs) and oral PMNs (oPMNs) taken from both controls and periodontitis patients. On average, 2.3% and 2.4% RANKL expression was detected on the cPMNs and oPMNs from periodontitis patients, which did not differ significantly from healthy controls. Since cPMNs may acquire a more osteoclastogenesis-facilitating phenotype while migrating into the inflamed periodontium, we next investigated whether stimulated (with LPS, TNF-α, or IL-6) cPMNs have the capacity to contribute to osteoclastogenesis. Enduring surface expression of RANKL for short-lived cells as cPMNs was achieved by fixating stimulated cPMNs. RANKL expression on stimulated cPMNs, as assessed by flow cytometry and immunohistochemistry, was limited (6.48±0.72%,mean expression±SEM) after 24 and 48 hours of stimulation with LPS. Likewise, stimulation with TNF-αand IL-6 resulted in limited RANKL expression levels. These limited levels of expression did not induce osteoclastogenesis when cocultured with preosteoclasts for 10 days. We report that, under the aforementioned experimental conditions, neither cPMNs nor oPMNs directly induced osteoclastogenesis. Further elucidation of the key cellular players and immune mediators that stimulate alveolar bone resorption in periodontitis will help to unravel its pathogenesis.


2020 ◽  
Vol 14 (1) ◽  
pp. 82-87
Author(s):  
Susi R. Puspitadewi ◽  
Lindawati S. Kusdhany ◽  
Sri Lelyati C. Masulili ◽  
Pitu Wulandari ◽  
Hanna B. Iskandar ◽  
...  

Background: Postmenopausal women exhibit reduced bone mineralization, which causes bone resorption, including that of alveolar bone. Parathyroid hormone has been shown to play a role in alveolar bone resorption. Objective: This study aims to analyze relationships between parathyroid hormone and other factors that may contribute to alveolar bone resorption in postmenopausal women. Methods: This cross-sectional study included 82 postmenopausal women aged 50–74 years, who resided in Central and East Jakarta, Indonesia. Subjects' data were obtained through questionnaires, dental examinations, and blood collection for the examination of parathyroid hormone levels by enzyme-linked immunosorbent assay and using panoramic radiography to measure bone resorption. Results: Spearman correlation analysis showed a significant correlation between parathyroid hormone level (p = 0.005) and extent of alveolar bone resorption, but age (p = 0.292), menopausal duration (p = 0.244), and number of missing teeth (p = 0.517) were not significantly correlated with the extent of alveolar bone resorption. Conclusion: Various factors play a role in the mechanism of bone resorption, so knowing the role of each factor is expected to reduce the effects of alveolar bone resorption that occurs in postmenopause. Among the factors investigated in this study, the parathyroid hormone was the sole factor correlated with postmenopausal alveolar bone resorption.


1987 ◽  
Vol 66 (12) ◽  
pp. 1753-1757 ◽  
Author(s):  
I. Nishimura ◽  
P.J. Damiani ◽  
D.A. Atwood

The post-extraction resorption of residual ridges (RRR) is a major and largely unsolved health problem, probably of multifactorial etiology. In order for one to study the role of specific factors in the pathophysiology of RRR, the use of animal models is desirable. The purpose of this study was to establish a reliable animal model and a standardized assay system to measure RRR for future experiments. A new oblique cephalometric device was designed to take pairs of xeroradiographs on the right and left sides of the rat skull and mandible at a 45-degree angle to the horizontal plane. Preliminary studies confirmed the reproducibility of the technique. All molars were extracted with minimal trauma from the right maxilla and mandible in five male Sprague-Dawley rats (40 days old). Longitudinal cephalographic examinations were performed before and immediately after extraction and at two, four, eight, and 12 weeks after extraction. Alveolar bone resorption was measured on enlarged cephalographs (5. 7X) at a point mesial to the mandibular first molar. Sequential mean bone resorption was 0.8 ± 0.2 mm (S.D.), 1.0 ± 0.3, 1.3 ± 0.3, and 1.5 ± 0.4, respectively. Graphically, these findings produced bone loss curves similar to those observed in man. These results indicate that the rat model may be utilized in longitudinal studies of the resorption of the residual ridge.


2021 ◽  
pp. 002203452110196
Author(s):  
J. Li ◽  
F. Jin ◽  
M. Cai ◽  
T. Lin ◽  
X. Wang ◽  
...  

Periodontitis is the most common chronic oral disease and is characterized by active osteoclast activity and significant alveolar bone resorption. However, the key regulatory factors of periodontal bone loss have yet to be determined, and reasonable intervention methods for periodontitis have not been developed. Currently, long noncoding RNAs (lncRNAs) have shown a remarkable ability to maintain normal cell and tissue homeostasis. Interestingly, we recently found that the lncRNA Nron is negatively correlated with alveolar bone resorption in periodontitis model. To explore the role of Nron in periodontal bone loss, osteoclastic-specific Nron knockout mice and osteoclastic-specific Nron transgenic mice were generated. Nron effectively inhibited osteoclastogenesis and alveolar bone resorption. Mechanistically, Nron was found to effectively promote the nuclear transport of NF-κb repressing factor (NKRF). In addition, NKRF in the nucleus significantly repressed the transcription of Nfatc1, which is a major NF-κb signaling molecule. Importantly, local injection of the Nron overexpression vector significantly inhibited osteoclastogenesis and alveolar bone resorption, which indicated the translational application potential of lncRNAs in the treatment of bone resorption in periodontitis.


2021 ◽  
pp. 002203452098477
Author(s):  
S. Wald ◽  
A. Leibowitz ◽  
Y. Aizenbud ◽  
Y. Saba ◽  
K. Zubeidat ◽  
...  

Sustained mechanical forces applied to tissue are known to shape local immunity. In the oral mucosa, mechanical stress, either naturally induced by masticatory forces or externally via mechanical loading during orthodontic tooth movement (OTM), is translated, in part, by T cells to alveolar bone resorption. Nevertheless, despite being considered critical for OTM, depletion of CD4+ and CD8+ T cells is reported to have no impact on tooth movement, thus questioning the function of αβT cells in OTM-associated bone resorption. To further address the role of T cells in OTM, we first characterized the leukocytes residing in the periodontal ligament (PDL), the tissue of interest during OTM, and compared it to the neighboring gingiva. Unlike the gingiva, monocytes and neutrophils represent the major leukocytes of the PDL. These myeloid cells were also the main leukocytes in the PDL of germ-free mice, although at lower levels than SPF mice. T lymphocytes were more enriched in the gingiva than the PDL, yet in both tissues, the relative fraction of the γδT cells was higher than the αβ T cells. We thus sought to examine the role of γδT cells in OTM. γδT cells residing in the PDL were mainly Vγ6+ and produced interleukin (IL)–17A but not interferon-γ. Using Tcrd-GDL mice allowing conditional ablation of γδT cells in vivo, we demonstrate that OTM was greatly diminished in the absence of γδT cells. Further analysis revealed that ablation of γδT cells decreased early IL-17A expression, monocyte and neutrophil recruitment, and the expression of the osteoclastogenic molecule receptor activator of nuclear factor–κβ ligand. This, eventually, resulted in reduced numbers of osteoclasts in the pressure site during OTM. Collectively, our data suggest that γδT cells are essential in OTM for translating orthodontic mechanical forces to bone resorption, required for relocating the tooth in the alveolar bone.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Alexandra Cloitre ◽  
Boris Halgand ◽  
Sophie Sourice ◽  
Jocelyne Caillon ◽  
Olivier Huck ◽  
...  

AbstractPeriodontitis is a prevalent chronic inflammatory disease due to the host response (IL-1β, IL-6, TNF-α and IL-17A) to oral bacteria such as Porphyromonas gingivalis. The newer members of the IL-1 family, IL-36s (IL-36α/IL-36β/IL-36γ/IL-36Ra/IL-38) are known to be involved in host defense against P. gingivalis in oral epithelial cells (OECs) and are considered as key inflammatory mediators in chronic diseases. The aim of this study was to investigate the potential role of IL-36s in periodontitis. We showed here that IL-36γ mRNA gingival expression is higher in periodontitis patients, whereas IL-36β and IL-36Ra mRNA expression are lower compared to healthy controls. Interestingly, the elevated IL-36γ expression in patients is positively correlated with the RANKL/OPG ratio, an index of bone resorption. In vitro, IL-36γ expression was induced through TLR2 activation in primary OECs infected with P. gingivalis but not in gingival fibroblasts, the most widespread cell type in gingival connective tissue. In OECs, recombinant IL-36γ enhanced the expression of inflammatory cytokines (IL-1β, IL-6, TNF-α and IL-36γ), of TLR2 and importantly, the RANKL/OPG ratio. These findings suggest that IL-36γ could be a pivotal inflammatory player in periodontitis by perpetuating gingival inflammation and its associated alveolar bone resorption and could be a relevant therapeutic target.


2017 ◽  
Vol 26 (3) ◽  
pp. 107-114
Author(s):  
Dan Piperea-Sianu ◽  
◽  
Adela M. Ceau ◽  
Mara Carsote ◽  
Alexandru G. Croitoru ◽  
...  

Osteoporosis and periodontal disease (PD) are two chronic diseases, characterized by bone loss, with systemic or local impact (alveolar bone). Both pathologies have a progressive evolution, leading to systemic bone loss in the case of osteoporosis and bone lysis localized in the alveolar bone in the case of periodontal disease. The present paper presents recent data from the literature on the association between periodontal disease and osteoporosis, on the role of cytokines in the bone resorption-apposition imbalance, and on how periodontal disease causes changes in serum levels of cytokines, leading to disorders in the systemic bone formation. We also found it useful, especially for rheumatologists, to outline the extent to which periodontal disease can create a systemic context favorable to the development of osteoporosis.


2019 ◽  
Vol 7 (1) ◽  
pp. 18 ◽  
Author(s):  
Ronald B. Brown

An association between periodontal disease and cancer has been established in recent studies, but no common etiology has been identified in the hopes of reducing the global burden of these non-communicable diseases. This perspective article hypothesizes that the determinant mediating the association of periodontal disease with cancer is dysregulated phosphate metabolism. Phosphate, an essential dietary micronutrient, is dysregulated in chronic kidney disease, and both cancer and periodontal disease are associated with chronic kidney disease. Reviewed evidence includes the association between phosphate toxicity and cancer development, and the association between periodontal disease and chronic kidney disease-mineral and bone disorder includes conditions such as ectopic calcification and bone resorption, which may be indirectly related to periodontal disease. Dental calculus in periodontal disease contains calcium phosphate crystals that are deposited from excess calcium and phosphate in saliva. Alveolar bone resorption may be linked systemically to release of parathyroid hormone in response to hypocalcemia induced by hyperphosphatemia. More research is needed to examine the role of dysregulated phosphate metabolism in periodontal disease.


2014 ◽  
Vol 56 (2) ◽  
pp. 54-57 ◽  
Author(s):  
Takenori Sato ◽  
Kiyoko Watanabe ◽  
Toshizo Toyama ◽  
Hidefumi Kumada ◽  
Haruka Sasaki ◽  
...  

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