Computational simulations of endocrine bone diseases related to pathological glandular PTH secretion using a multi-scale bone cell population model.

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 implemen

SUBMITTER: Modiz C 

PROVIDER: S-EPMC12521151 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature