scholarly journals Osteoporosis: From Molecular Mechanisms to Therapies

2020 ◽  
Vol 21 (3) ◽  
pp. 714 ◽  
Author(s):  
Chih-Hsin Tang
Keyword(s):  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Molecular Mechanisms ◽  
Current Understanding ◽  
Special Issue ◽  
Anabolic Agents ◽  
Trabecular Microarchitecture ◽  
Stimulate Bone Formation ◽  
Skeletal Disorder

Osteoporosis is a common skeletal disorder, occurring as a result of an imbalance between bone resorption and bone formation, with bone breakdown exceeding bone building. Bone resorption inhibitors, e.g., bisphosphonates, have been designed to treat osteoporosis, while anabolic agents such as teriparatide stimulate bone formation and correct the characteristic changes in the trabecular microarchitecture. However, all of these drugs are associated with significant side effects. It is therefore crucial that we continue to research the pathogenesis of osteoporosis and seek novel modes of therapy. This editorial summarizes and discusses the themes of the fifteen articles published in the Special Issue, Osteoporosis: From Molecular Mechanisms to Therapies 2019, as part of the global picture of the current understanding of osteoporosis.

scholarly journals Osteoporosis: From Molecular Mechanisms to Therapies 2.0

2020 ◽  
Vol 21 (21) ◽  
pp. 8005
Author(s):  
Chih-Hsin Tang
Keyword(s):  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Molecular Mechanisms ◽  
Current Understanding ◽  
Special Issue ◽  
Trabecular Microarchitecture ◽  
Anabolic Agent ◽  
Skeletal Disorder

Osteoporosis is a common skeletal disorder, occurring as a result of an imbalance between bone resorption and bone formation, with bone breakdown exceeding bone building. Bone resorption inhibitors, e.g., bisphosphonates, have been designed to treat osteoporosis. Teriparatide, an anabolic agent, stimulates bone formation and corrects the characteristic changes in the trabecular microarchitecture. However, these drugs are associated with significant side effects. It is therefore crucial that we continue to research the pathogenesis of osteoporosis and seek novel modes of therapy. This editorial summarizes and discusses the themes of the ten articles published in our Special Issue “Osteoporosis: From Molecular Mechanisms to Therapies 2.0”, a continuation of our 2019 Special Issue "Osteoporosis: From Molecular Mechanisms to Therapies" (https://www.mdpi.com/journal/ijms/special_issues/osteoporosis_ijms). These Special Issues detail important global scientific findings that contribute to our current understanding of osteoporosis.

scholarly journals Osteoporosis: From Molecular Mechanisms to Therapies 3.0

2021 ◽  
Vol 22 (23) ◽  
pp. 12725
Author(s):  
Chih-Hsin Tang
Keyword(s):  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Molecular Mechanisms ◽  
Current Understanding ◽  
Special Issue ◽  
Trabecular Microarchitecture ◽  
Anabolic Agent ◽  
Skeletal Disorder

Osteoporosis is a common skeletal disorder that occurs as a result of an imbalance between bone resorption and bone formation, with bone breakdown exceeding bone building. Bone resorption inhibitors, e.g., bisphosphonates, have been designed to treat osteoporosis. Teriparatide, an anabolic agent, stimulates bone formation and corrects the characteristic changes in the trabecular microarchitecture. However, these drugs are associated with significant side effects. It is therefore crucial that we continue to research the pathogenesis of osteoporosis and seek novel modes of therapy. This editorial summarizes and discusses the themes of the six articles published in our Special Issue “Osteoporosis: From Molecular Mechanisms to Therapies 3.0”, a continuation of our 2020 Special Issue "Osteoporosis: From Molecular Mechanisms to Therapies". These Special Issues detail important global scientific findings that contribute to our current understanding of osteoporosis.

scholarly journals Overview on the Side Effects of Doxorubicin

2020 ◽  
Author(s):  
Chittipolu Ajaykumar
Keyword(s):  
Side Effects ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Cytotoxic Effect ◽  
Molecular Mechanisms ◽  
Current Understanding ◽  
Preventive Strategies ◽  
Normal Cells ◽  
Dna Strand

Doxorubicin is an anthracycline antibiotic extracted from the bacterium Streptomyces peucetius. Its cytotoxic effect produced by intercalating with DNA causing breakdown of DNA strand which causes cancer cell apoptosis. Despite being an effective anticancer agent it causes several crucial side effects like carditoxicity, neuropathy, hepatotoxicity, nephrotoxicity, alopecia, typhlitis, myelosuppression, neutropenia, anaemia, thrombocytopenia, nausea, and diarrhoea were caused mainly due to the inability to distinguish between cancer cells and normal cells. This chapter mainly focuses on doxorubicin’s side effects, current understanding of the molecular mechanisms, and management and preventive strategies of doxorubicin’s cardiotoxicity during the treatment of various type of cancer.

scholarly journals SCREENING FOR VIETNAMESE PLANT EXTRACTS WITH POTENTIAL BENEFIT FOR ANTI OSTEOCLASTOGENESISH

2021 ◽  
Vol 59 (4) ◽  
pp. 507
Author(s):  
Hai Dang Nguyen ◽  
Thanh Huong Le ◽  
Thu Trang Duong
Keyword(s):  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Plant Extracts ◽  
Potential Benefit ◽  
Mouse Macrophage ◽  
Potential Source ◽  
Inhibitory Activities ◽  
First Time

Bone's homeostasis is only achieved when there is a balance between bone formation and bone resorption. A metabolic disorder of bone-resorbing osteoclasts can lead to osteoporosis. Long-term use of anti-osteoporosis drugs can lead to undesirable side effects so traditional herbal can be a potential source of alternative medicine. In the present study, forty one Vietnamese plants (seventy methanol extracts) were screened for osteoclastogenesis inhibitory activities on RAW264.7 mouse macrophage cells. For the first time, 29 extracts from 24 species showed potential as effective inhibitors of osteoclastogenesis.

scholarly journals New Insights Into the Physiology of Bone Regulation: the Role of Neurohormones

2014 ◽  
pp. 421-427 ◽  
Author(s):  
I. ŽOFKOVÁ ◽  
P. MATUCHA
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Bone Metabolism ◽  
Bone Tissue ◽  
Protective Effects ◽  
Humoral Factors ◽  
Stimulate Bone Formation ◽  
Osteoblast Activity ◽  
Beta 2

Bone metabolism is regulated by interaction between two skeletal cells – osteoclasts and osteoblasts. Function of these cells is controlled by a number of humoral factors, including neurohormones, which ensure equilibrium between bone resorption and bone formation. Influence of neurohormones on bone metabolism is often bimodal and depends on the tissue, in which the hormone is expressed. While hypothalamic beta-1 and beta-2-adrenergic systems stimulate bone formation, beta-2 receptors in bone tissue activate osteoclatogenesis and increases bone resorption. Chronic stimulation of peripheral beta-2 receptors is known to quicken bone loss and alter the mechanical quality of the skeleton. This is supported by the observation of a low incidence of hip fractures in patients treated with betablockers. A bimodal osteo-tropic effect has also been observed with serotonin. While serotonin synthetized in brain has osteo-anabolic effects, serotonin released from the duodenum inhibits osteoblast activity and decreases bone formation. On the other hand, both cannabinoid systems (CB1 receptors in the brain and CB2 in bone tissue) are unambiguously osteo-protective, especially with regard to the aging skeleton. Positive (protective) effects on bone have also been shown by some hypophyseal hormones, such as thyrotropin (which inhibits bone resorption) and adrenocorticotropic hormone and oxytocin, both of which stimulate bone formation. Low oxytocin levels have been shown to potentiate bone loss induced by hypoestrinism in postmenopausal women, as well as in girls with mental anorexia. In addition to reviewing neurohormones with anabolic effects, this article also reviews neurohormones with unambiguously catabolic effects on the skeleton, such as neuropeptide Y and neuromedin U. An important aim of research in this field is the synthesis of new molecules that can stimulate osteo-anabolic or inhibiting osteo-catabolic processes.

scholarly journals Molecular understanding of pharmacological treatment of osteoporosis

2019 ◽  
Vol 4 (4) ◽  
pp. 158-164 ◽  
Author(s):  
Sakae Tanaka
Keyword(s):  
Bone Resorption ◽  
Bone Formation ◽  
Bone Turnover ◽  
Pharmacological Treatment ◽  
Bone Remodelling ◽  
Health Concern ◽  
Anabolic Agents ◽  
Treatment Of Osteoporosis ◽  
Turnover Process ◽  
Skeletal Integrity

Osteoporosis is a serious health concern, particularly in aged societies. The burden of osteoporosis with its associated morbidity and mortality due to fracture has become a critical socioeconomic problem. Skeletal integrity is maintained through a balance of bone resorption and bone formation. The bone turnover process, called bone remodelling. Recently, a number of anti-osteoporosis drugs with excellent anti-osteoporosis and fracture effects have been developed. They are mainly classified into two groups according to their effects on bone remodelling: anti-resorptive agents and anabolic agents. Cite this article: EFORT Open Rev 2019;4:158-164. DOI: 10.1302/2058-5241.4.180018

scholarly journals Research of Pathogenesis and Novel Therapeutics in Arthritis

2019 ◽  
Vol 20 (7) ◽  
pp. 1646 ◽  
Author(s):  
Chih-Hsin Tang
Keyword(s):  
Rheumatoid Arthritis ◽  
Psoriatic Arthritis ◽  
Side Effects ◽  
Inflammatory Arthritis ◽  
Current Understanding ◽  
Special Issue ◽  
Novel Therapeutics ◽  
High Prevalence ◽  
Exact Etiology ◽  
Inflammatory Drugs

Arthritis has a high prevalence globally and includes over 100 types, the most common of which are rheumatoid arthritis, osteoarthritis, psoriatic arthritis and inflammatory arthritis. The exact etiology of arthritis remains unclear and no cure exists. Anti-inflammatory drugs are commonly used in the treatment of arthritis, but are associated with significant side effects. Novel modes of therapy and additional prognostic biomarkers are urgently needed for these patients. In this editorial, the twenty articles published in the Special Issue Research of Pathogenesis and Novel Therapeutics in Arthritis 2019 are summarized and discussed as part of the global picture of the current understanding of arthritis.

scholarly journals Transcriptomics‐based analysis of the mechanism by which Wang-Bi capsule alleviates joint destruction in rats with collagen‐induced arthritis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Haiyang Shu ◽  
Hanxiao Zhao ◽  
Yingjie Shi ◽  
Cheng Lu ◽  
Li Li ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Formation ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Joint Destruction ◽  
Micro Ct ◽  
Collagen Induced Arthritis ◽  
Cartilage Development ◽  
And Cartilage

Abstract Background Rheumatoid arthritis (RA) is a chronic autoimmune disease accompanied with joint destruction that often leads to disability. Wang-Bi capsule (WB), a traditional Chinese medicine-based herbs formula, has exhibited inhibition effect on joint destruction of collagen-induced arthritis (CIA) animal model in our previous study. But its molecular mechanisms are still obscure. Methods CIA rats were treated intragastrical with WB for eight weeks, and the effect of joints protection were evaluated by hematoxylin and eosin (H&E) staining, safranin O fast green staining, tartrate-resistant acid phosphatase (TRAP) staining and micro‑CT scanning analysis. The transcriptomic of tarsal joints were used to investigate how WB alleviated joint destruction. Results The histological examination of ankle joints showed WB alleviated both cartilage damage and bone destruction of CIA rats. This protective effect on joints were further evidenced by micro-CT analysis. The transcriptomic analysis showed that WB prominently changed 12 KEGG signaling pathways (“calcium signaling pathway”, “cAMP signaling pathway”, “cell adhesion molecules”, “chemokine signaling pathway”, “complement and coagulation cascades”, “MAPK signaling pathway”, “NF-kappa B signaling pathway”, “osteoclast differentiation”, “PI3K-Akt signaling pathway”, “focal adhesion”, “Gap junction” and “Rap1 signaling pathway”) associated with bone or cartilage. Several genes (including Il6, Tnfsf11, Ffar2, Plg, Tnfrsf11b, Fgf4, Fpr1, Siglec1, Vegfd, Cldn1, Cxcl13, Chad, Arrb2, Fgf9, Egfr) regulating bone resorption, bone formation and cartilage development were identified by further analysis. Meanwhile, these differentially expressed genes were validated by real-time quantitative PCR. Conclusions Overall, the protective effect of WB treatment on joint were confirmed in CIA rats, and its basic molecular mechanisms may be associated with regulating some genes (including Il6, Tnfsf11, Ffar2 and Plg etc.) involved in bone resorption, bone formation and cartilage development.

scholarly journals Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism

2020 ◽  
Vol 47 (4) ◽  
pp. 75-80
Author(s):  
I. Yankova ◽  
A. Shinkov ◽  
R. Kovatcheva
Keyword(s):  
Bone Resorption ◽  
Primary Hyperparathyroidism ◽  
Bone Formation ◽  
Bone Metabolism ◽  
Cortical Bone ◽  
Mineral Density ◽  
Trabecular Microarchitecture ◽  
Duration Of Action ◽  
Increased Risk ◽  
Stimulation Of

AbstractParathyroid hormone (PTH) is a key regulator of bone turnover. Depending on the duration of action, the hormone causes catabolic and anabolic effects by binding with specific receptors (PTHR1) in the bone. Various cells expressing PTHR1 on their surface are involved in the process – osteoblasts, osteocytes, bone marrow stromal cells, T-lymphocytes and macrophages. In physiological conditions PTH balances the bone metabolism. Intermittent pharmacological doses of PTH lead to the prevalence of bone formation and are used in the treatment of osteoporosis. Persistently elevated levels of PTH stimulate bone resorption by impacting mainly the cortical bone. New imaging and analysis techniques show that high PTH levels can also have an adverse effect on trabecular microarchitecture. Primary hyperparathyroidism (PHPT) is a disease characterized by increased bone metabolism, decreased bone mineral density (BMD), inadequate osteoid mineralization and an increased risk of fractures. Prolonged overproduction of PTH leads to stimulation of bone resorption and defects in bone formation, mainly causing loss of cortical bone mass, while in the trabecular bone predominate demineralization processes. One explanation of these findings is the enhanced stimulation of RANKL expression by osteoblasts with decreased OPG expression and bone formation at the same time.

scholarly journals Effect of low-dose of recombinant human growth hormone on bone metabolism in elderly women with osteoporosis

2002 ◽  
pp. 339-348 ◽  
Author(s):  
T Sugimoto ◽  
H Kaji ◽  
D Nakaoka ◽  
M Yamauchi ◽  
S Yano ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Lumbar Spine ◽  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Low Dose ◽  
Elderly Women ◽  
Serum Concentrations ◽  
Gh Treatment ◽  
Igf I

BACKGROUND: There has been increasing evidence that the growth hormone (GH)-IGF-I axis plays an important part in the maintenance of bone mass. However, controversy still exists as to the effect of GH treatment on bone mineral density (BMD) in elderly patients with osteoporosis. OBJECTIVE: To investigate the effect of low-dose GH treatment on markers of body composition and bone turnover, serum concentrations of IGF-I and IGF-binding proteins (IGFBPs), and BMD at the radius and lumbar spine in eight elderly Japanese women with osteoporosis. METHODS: Participants were treated with GH as a single daily subcutaneous injection (0.125 IU/kg per week; 0.00595 mg/kg per day) for 48 weeks. RESULTS: Markers of bone formation and bone resorption were both increased up to 24 weeks of GH treatment. The bone formation markers remained increased during GH treatment, whereas the bone resorption markers returned to baseline values after 24 weeks of GH treatment. GH treatment caused a rapid (within 2 weeks) and sustained increase in serum IGF-I concentration. As for IGFBPs, serum concentrations of IGFBPs-2, -3 and -4 did not change significantly during GH treatment. In contrast, GH treatment caused a gradual increase in serum IGFBP-5 concentration, with a significant increase seen 48 weeks after the start of GH treatment. Radial BMD seemed to be increased during the late period of GH treatment, although the change was not significant. Lumbar BMD did not change during GH treatment. GH treatment caused a significant increase in hand grip strength. None of the GH-treated participants had new fractures and side effects such as edema and joint pain. Radial BMD was significantly increased after discontinuation of GH treatment for another 48 weeks and a similar tendency was observed at the lumbar spine (7.1+/-2.3% above pretreatment values for the radius and 3.6+/-2.0% for the lumbar spine). CONCLUSIONS: Low-dose GH treatment attenuated the decrease in muscle strength and bone mass in elderly women without side effects, although changes in nutrition and exercise might affect BMD. The present findings provide useful information regarding the use of low-dose GH treatment in elderly women with osteoporosis.

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