ReviewBiomedicines2024
Mechanistic Insights and Therapeutic Strategies in Osteoporosis: A Comprehensive Review.
Review in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- MRONJ Risk Related to Dental Implants in Osteoporosis Treated With Denosumab: A Systematic Review.Oral diseases · 2026Pooled it
- Meta-analysis of the effects of probiotic supplementation on bone turnover markers in middle-aged and elderly patients with osteoporosis.Frontiers in cellular and infection microbiology · 2025Pooled it
- Long non-coding RNA antisense of insulin-like growth factor 2 receptor promotes osteogenic differentiation by enhancing runt-related transcription factor 2 translation: A potential therapeutic target for osteoporosis.Journal of advanced research · 2026Article
- Article
- Article
- Osteocytes in the Metastatic Bone Niche: Mechanistic Pathways and Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Lacticaseibacillus rhamnosus LGG Suppresses Osteoclastogenesis via TLR6/NF-κB Modulation and Attenuates Ovariectomy-Induced Bone Loss in Mice.Probiotics and antimicrobial proteins · 2026Article
- Therapeutic potential of fish collagen hydrolysates in osteoporosis prevention: a narrative review based on cellular, molecular, and clinical evidence.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Review
- Review
- Cell-penetrating H3 tail peptides suppress osteoclast differentiation via inhibition of MMP-9-mediated histone H3 clipping.BMB reports · 2026Article
- Enhancing osteoporosis treatment: emerging roles of engineered exosomes in bone regeneration and repair.Journal of translational medicine · 2026Review
- Combined Nanoparticle-Based Delivery of Estrogens and Raloxifen in Postmenopausal Osteoporosis.Nanomaterials (Basel, Switzerland) · 2026Review
- Modulation of tocotrienol's bone effects by osteocytes: a perspective.Frontiers in pharmacology · 2026Article
- Free amino acid-rich egg yolk protein hydrolysate promotes osteogenesis of MC3T3-E1 cells association withFrontiers in nutrition · 2026Article
- Advances in the regulation of bone metabolism by central nuclei: a new perspective on the brain-bone axis.Frontiers in neuroscience · 2026Review
- Apelin promotes RANKL‑mediated osteoclastogenesis by activating MAPK and NF‑κB pathways.Molecular medicine reports · 2026Article
- Review
- [Antiresorptive therapies in osteoporosis].Orthopadie (Heidelberg, Germany) · 2025Review
- Modern Strategies for Osteoporosis Therapy: Current Status and Prospects for Targeted Intervention.International journal of molecular sciences · 2025Review
- Effect of combined exercise and nutrition on bone density in postmenopausal women-a systematic review and meta-analysis.Nutrition & metabolism · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis, a metabolic bone disorder characterized by decreased bone mass per unit volume, poses a significant global health burden due to its association with heightened fracture risk and adverse impacts on patients' quality of life. This review synthesizes the current understanding of the pathophysiological mechanisms underlying osteoporosis, with a focus on key regulatory pathways governing osteoblast and osteoclast activities. These pathways include RANK/RANKL/OPG, Wingless-int (Wnt)/β-catenin, and Jagged1/Notch1 signaling, alongside the involvement of parathyroid hormone (PTH) signaling, cytokine networks, and kynurenine in bone remodeling. Pharmacotherapeutic interventions targeting these pathways play a pivotal role in osteoporosis management. Anti-resorptive agents, such as bisphosphonates, estrogen replacement therapy/hormone replacement therapy (ERT/HRT), selective estrogen receptor modulators (SERMs), calcitonin, anti-RANKL antibodies, and cathepsin K inhibitors, aim to mitigate bone resorption. Conversely, anabolic agents, including PTH and anti-sclerostin drugs, stimulate bone formation. In addition to pharmacotherapy, nutritional supplementation with calcium, vitamin D, and vitamin K2 holds promise for osteoporosis prevention. However, despite the availability of therapeutic options, a substantial proportion of osteoporotic patients remain untreated, highlighting the need for improved clinical management strategies. This comprehensive review aims to provide clinicians and researchers with a mechanistic understanding of osteoporosis pathogenesis and the therapeutic mechanisms of existing medications. By elucidating these insights, this review seeks to inform evidence-based decision-making and optimize therapeutic outcomes for patients with osteoporosis.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.