scholarly journals How does the viability of bone-restricted osteocytes regulate bone atrophy?

2021 ◽  
Vol 10 (1) ◽  
pp. 64-65
Author(s):  
Aline (Prof. Dr) Bozec ◽  
Darja (Dr) Andreev ◽  
Friedrich Alexander

How does the viability of bone-restricted osteocytes regulate bone atrophy? Osteocyte death is amplified in many bone diseases and is ubiquitous upon ageing. To date, the impact of osteocyte death on pathological bone loss is poorly studied due to the remote location of osteocytes. Within the ERC Starting Grant project “Unknown functions of Osteocyte DEath (ODE)” we will make use of new imaging and omics technologies to unravel this question.

2021 ◽  
Vol 22 (2) ◽  
pp. 596
Author(s):  
Agnes Schröder ◽  
Joshua Gubernator ◽  
Alexandra Leikam ◽  
Ute Nazet ◽  
Fabian Cieplik ◽  
...  

Dietary salt uptake and inflammation promote sodium accumulation in tissues, thereby modulating cells like macrophages and fibroblasts. Previous studies showed salt effects on periodontal ligament fibroblasts and on bone metabolism by expression of nuclear factor of activated T-cells-5 (NFAT-5). Here, we investigated the impact of salt and NFAT-5 on osteoclast activity and orthodontic tooth movement (OTM). After treatment of osteoclasts without (NS) or with additional salt (HS), we analyzed gene expression and the release of tartrate-resistant acid phosphatase and calcium phosphate resorption. We kept wild-type mice and mice lacking NFAT-5 in myeloid cells either on a low, normal or high salt diet and inserted an elastic band between the first and second molar to induce OTM. We analyzed the expression of genes involved in bone metabolism, periodontal bone loss, OTM and bone density. Osteoclast activity was increased upon HS treatment. HS promoted periodontal bone loss and OTM and was associated with reduced bone density. Deletion of NFAT-5 led to increased osteoclast activity with NS, whereas we detected impaired OTM in mice. Dietary salt uptake seems to accelerate OTM and induce periodontal bone loss due to reduced bone density, which may be attributed to enhanced osteoclast activity. NFAT-5 influences this reaction to HS, as we detected impaired OTM and osteoclast activity upon deletion.


2021 ◽  
Vol 22 (5) ◽  
pp. 2303
Author(s):  
Liang Li ◽  
Ming Yang ◽  
Saroj Kumar Shrestha ◽  
Hyoungsu Kim ◽  
William H. Gerwick ◽  
...  

Osteoclasts, bone-specified multinucleated cells produced by monocyte/macrophage, are involved in numerous bone destructive diseases such as arthritis, osteoporosis, and inflammation-induced bone loss. The osteoclast differentiation mechanism suggests a possible strategy to treat bone diseases. In this regard, we recently examined the in vivo impact of kalkitoxin (KT), a marine product obtained from the marine cyanobacterium Moorena producens (previously Lyngbya majuscula), on the macrophage colony-stimulating factor (M-CSF) and on the receptor activator of nuclear factor κB ligand (RANKL)-stimulated in vitro osteoclastogenesis and inflammation-mediated bone loss. We have now examined the molecular mechanism of KT in greater detail. KT decreased RANKL-induced bone marrow-derived macrophages (BMMs) tartrate-resistant acid phosphatase (TRAP)-multinucleated cells at a late stage. Likewise, KT suppressed RANKL-induced pit area and actin ring formation in BMM cells. Additionally, KT inhibited several RANKL-induced genes such as cathepsin K, matrix metalloproteinase (MMP-9), TRAP, and dendritic cell-specific transmembrane protein (DC-STAMP). In line with these results, RANKL stimulated both genes and protein expression of c-Fos and nuclear factor of activated T cells (NFATc1), and this was also suppressed by KT. Moreover, KT markedly decreased RANKL-induced p-ERK1/2 and p-JNK pathways at different time points. As a result, KT prevented inflammatory bone loss in mice, such as bone mineral density (BMD) and osteoclast differentiation markers. These experiments demonstrated that KT markedly inhibited osteoclast formation and inflammatory bone loss through NFATc1 and mitogen-activated protein kinase (MAPK) signaling pathways. Therefore, KT may have potential as a treatment for destructive bone diseases.


2021 ◽  
Vol 9 (3) ◽  
pp. 663
Author(s):  
Imran Farooq ◽  
Tara J. Moriarty

Tick-borne infectious diseases can affect many tissues and organs including bone, one of the most multifunctional structures in the human body. There is a scarcity of data regarding the impact of tick-borne pathogens on bone. The aim of this review was to survey existing research literature on this topic. The search was performed using PubMed and Google Scholar search engines. From our search, we were able to find evidence of eight tick-borne diseases (Anaplasmosis, Ehrlichiosis, Babesiosis, Lyme disease, Bourbon virus disease, Colorado tick fever disease, Tick-borne encephalitis, and Crimean–Congo hemorrhagic fever) affecting the bone. Pathological bone effects most commonly associated with tick-borne infections were disruption of bone marrow function and bone loss. Most research to date on the effects of tick-borne pathogen infections on bone has been quite preliminary. Further investigation of this topic is warranted.


2020 ◽  
Vol 22 (1) ◽  
pp. 222
Author(s):  
Eun-Nam Kim ◽  
Ga-Ram Kim ◽  
Jae Sik Yu ◽  
Ki Hyun Kim ◽  
Gil-Saeng Jeong

In bone homeostasis, bone loss due to excessive osteoclasts and inflammation or osteolysis in the bone formation process cause bone diseases such as osteoporosis. Suppressing the accompanying oxidative stress such as ROS in this process is an important treatment strategy for bone disease. Therefore, in this study, the effect of (2R)-4-(4-hydroxyphenyl)-2-butanol 2-O-β-d-apiofuranosyl-(1→6)-β-d-glucopyranoside (BAG), an arylbutanoid glycoside isolated from Betula platyphylla var. japonica was investigated in RANKL-induced RAW264.7 cells and LPS-stimulated MC3E3-T1 cells. BAG inhibited the activity of TRAP, an important marker of osteoclast differentiation and F-actin ring formation, which has osteospecific structure. In addition, the protein and gene levels were suppressed of integrin β3 and CCL4, which play an important role in the osteoclast-induced bone resorption and migration of osteoclasts, and inhibited the production of ROS and restored the expression of antioxidant enzymes such as SOD and CAT lost by RANKL. The inhibitory effect of BAG on osteoclast differentiation and ROS production appears to be due to the inhibition of MAPKs phosphorylation and NF-κβ translocation, which play a major role in osteoclast differentiation. In addition, BAG inhibited ROS generated by LPS and effectively restores the mineralization of lost osteoblasts, thereby showing the effect of bone formation in the inflammatory situation accompanying bone loss by excessive osteoclasts, suggesting its potential as a new natural product-derived bone disease treatment.


2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Megumi Kobayashi ◽  
Kenta Watanabe ◽  
Satoshi Yokoyama ◽  
Chiho Matsumoto ◽  
Michiko Hirata ◽  
...  

Capsaicin, a transient receptor potential vanilloid type 1 (TRPV1) ligand, regulates nerve-related pain-sensitive signals, inflammation, and cancer growth. Capsaicin suppresses interleukin-1-induced osteoclast differentiation, but its roles in bone tissues and bone diseases are not known. This study examined the effects of capsaicin on inflammatory bone resorption and prostaglandin E (PGE) production induced by lipopolysaccharide (LPS) in vitro and on bone mass in LPS-treated mice in vivo. Capsaicin suppressed osteoclast formation, bone resorption, and PGE production induced by LPS in vitro. Capsaicin suppressed the expression of cyclooxygenase-2 (COX-2) and membrane-bound PGE synthase-1 (mPGES-1) mRNAs and PGE production induced by LPS in osteoblasts. Capsaicin may suppress PGE production by inhibiting the expression of COX-2 and mPGES-1 in osteoblasts and LPS-induced bone resorption by TRPV1 signals because osteoblasts express TRPV1. LPS treatment markedly induced bone loss in the femur in mice, and capsaicin significantly restored the inflammatory bone loss induced by LPS in mice. TRPV1 ligands like capsaicin may therefore be potentially useful as clinical drugs targeting bone diseases associated with inflammatory bone resorption.


2021 ◽  
Vol 31 (3) ◽  
pp. 201-205
Author(s):  
Abdulla Varoneckas ◽  
Rokas Poška ◽  
Rokas Gelažius

Relevance of the problem. Over the years, dental implant placement has proven to be a routine and reliable procedure. Osteotomy site preparation has a significant impact on implantation success rate. Surgery using piezosurgery is used as an alternative method for osteotomy. Piezosurgery concept has proven to reduce mechanical and thermal tissue trauma. Aim. Compare clinical differences between piezosurgery (PS) and standard drilling (SD) in dental implantation. Materials and methods: A systematic review was based on the PRISMA guidelines. Search was carried out in electronic databases. Researched studies were observational, published less than 10 years ago, in English. Studies that involved immediate implantation or bone augmentation were excluded, as well as patients with metabolic bone diseases or using bisphosphonate therapy. Results. Regarding crestal bone loss, 3 out of 4 articles stated that there were no statistically significant differences between standard drilling and piezosurgery group. One study, however, disclosed that piezosurgery showed better preservation of crestal bone after 3 years. 5 studies measured primary stability and did not find any significant differences. Secondary stability, however, was significantly higher in the piezosurgery group at 2nd and 3rd months. 5 studies that measured the duration of surgeries reported longer osteotomy time for the piezosurgery group. Pain level on VAS scale, oppositely, was lower in piezosurgery group. Conclusion. In conclusion, piezosurgery can be considered as an alternative to standard drilling. In terms of success rate, crestal bone loss and primary stability, results seem to be very similar in both groups. Piezosurgery, although, seems to be advantageous achieving secondary stability and maintaining lower pain levels during the healing process.


Author(s):  
Ad. A. Mamedov ◽  
T. V. Timoshenko ◽  
T. S. Gutnikova

Relevance. The article studies the primary canine premature extraction as the cause of three-dimensional (sagittal, transversal, vertical) bone underdevelopment in the area of the extracted tooth. The research is relevant as there are insufficient data in the scientific literature on this topic and the prevalence of premature primary canine extraction for therapeutic and orthodontic indications is high.Materials and methods. The present case study developed a special technique for bone volume measurement in all planes by CBCT.Results. Several CBCTs of one patient over the period of three years were analyzed according to the suggested technique. The calculations demonstrated significant sagittal and vertical bone loss.Conclusions. The results of the research allowed us to conclude that premature extraction of the primary canines leads to the significant sagittal and vertical bone loss. Besides, no increase in the intercanine distance was detected despite the patient’s growth spurt.


2019 ◽  
Vol 8 (4) ◽  
pp. 431 ◽  
Author(s):  
Mi Kim ◽  
Won Kim ◽  
Jae-Eun Byun ◽  
Jung Choi ◽  
Suk Yoon ◽  
...  

Overactivated osteoclasts lead to many bone diseases, including osteoporosis and rheumatoid arthritis. The p38 MAPK (p38) is an essential regulator of the receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis and bone loss. We previously reported TAT conjugated thioredoxin-interacting protein-derived peptide (TAT-TN13) as an inhibitor of p38 in hematopoietic stem cells (HSCs). Here, we examined the role of TAT-TN13 in the differentiation and function of osteoclasts. TAT-TN13 significantly suppressed RANKL-mediated differentiation of RAW 264.7 cells and bone marrow macrophages (BMMs) into osteoclasts. TAT-TN13 also inhibited the RANKL-induced activation of NF-κB and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), leading to the decreased expression of osteoclast-specific genes, including tartrate-resistant acid phosphatase (TRAP) and Cathepsin K. Additionally, TAT-TN13 treatment protected bone loss in ovariectomized (OVX) mice. Taken together, these results suggest that TAT-TN13 inhibits osteoclast differentiation by regulating the p38 and NF-κB signaling pathway; thus, it may be a useful agent for preventing or treating osteoporosis.


2020 ◽  
pp. 1-15
Author(s):  
Nicolas Fischer ◽  
Thomas Efferth

BACKGROUND: Grapevine (Vitis vinifera L.) as basis for winemaking is one of the most economically important plants in modern agriculture. As requirements in viticulture are increasing due to changing environments, terroir and pests, classical agriculture techniques reach their limits. OBJECTIVE: We summarize the impact of modern “omics” technologies on modern grapevine breeding and cultivation, as well as for dealing with challenges in viniculture caused by environmental or terroir changes and pests and diseases. In this review, we give an overview on current research on the influence of “omics” technologies on modern viticulture. RESULTS: Considerable advances in bioinformatics and analytical techniques such as next generation sequencing or mass spectrometry fueled new molecular biological studies. Modern “omics” technologies such as “genomics”, “transcriptomics”, “proteomics” and “metabolomics” allow the investigation on a large-scale data basis and the identification of key markers. Holistic understanding of genes, proteins and metabolites in combination with external biotic and abiotic factors improves vine and wine quality. CONCLUSION: The rapid evolution in wine quality was only enabled by the progress of modern biotechnological methods developing enology from a handcraft to science.


2015 ◽  
Vol 43 (03) ◽  
pp. 495-512 ◽  
Author(s):  
Ju-Young Kim ◽  
Sung-Jun Ahn ◽  
Jong Min Baek ◽  
Kwon-Ha Yoon ◽  
Myeung Su Lee ◽  
...  

The roots of Ostericum koreanum (OK) Maximowicz have traditionally been used to produce an herbal medicine reported to possess anti-inflammatory, anti-oxidant, antimicrobial, and antitumor activities; however, its effect on bone metabolism has not yet been reported. The present study examined the effects of OK extract on lipopolysaccharide (LPS)-induced bone loss in mice by investigating bone structure and the levels of the receptor activator of nuclear factor kappa-B ligand (RANKL) and osteoprotegerin (OPG) in serum and bone marrow fluid (BMF). The effects of OK extract on osteoclastogenesis were also investigated in mouse bone marrow macrophages by examining the formation of tartrate-resistant acid phosphatase (TRAP)-positive cells, the actin ring, and bone resorption activity. OK reduced LPS-induced bone destruction in vivo via a decrease in the RANKL/OPG ratio. Furthermore, it suppressed the formation of TRAP-positive cells and the actin ring, and reduced the bone-resorbing activity of mature osteoclasts. OK also significantly down-regulated the expression of various osteoclast-specific genes. However, it did not affect osteoblast differentiation, or the expression of genes involved in this process. These results demonstrated that OK prevented LPS-induced bone loss by decreasing the RANKL/OPG ratio in serum and BMF, and inhibited osteoclast differentiation and function, suggesting that OK represents a potential therapeutic drug for the treatment of osteoclast-associated bone diseases.


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