ArticleFrontiers in bioengineering and biotechnology2025
Computational simulations of endocrine bone diseases related to pathological glandular PTH secretion using a multi-scale bone cell population model.
Article in Frontiers in bioengineering and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The recent progression of extracellular vesicles application in osteoporosis.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Bone diseases significantly impact global health by compromising skeletal integrity and quality of life. In disease states linked to parathyroid hormone (PTH) glandular secretion, disrupted PTH patterns typically promote osteoclast proliferation, leading to increased bone resorption. Methods: While mathematical modeling has proven valuable in analyzing bone remodeling, current bone cell population models oversimplify PTH secretion by assuming constant levels, limiting their ability to represent disorders characterized by variations in PTH pulse characteristics. To address this, we present a novel semi-coupled approach integrating a two-state PTH receptor model with an established bone cell population model. Instead of conventional Hill-type functions, we implement a cellular activity function derived from the receptor model, incorporating pulsatile PTH patterns, cell dynamics, and intracellular communication pathways. Results: Our numerical simulations demonstrate the model's capability to reproduce various catabolic bone diseases, providing realistic changes in bone volume fraction over a 1-year period. Notably, while direct implementation of PTH disease progression in the bone cell population model fails to capture diseases only characterized by altered pulse duration and baseline, such as glucocorticoid-induced osteoporosis, our semi-coupled approach successfully models these conditions. Discussion: This physiologically more realistic approach to endocrine disease modeling offers potential implications for optimizing therapeutic interventions and understanding disease progression mechanisms.
Indexed as
Identifiers
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.