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Related Concept Videos

Hormones and Bone Tissue01:17

Hormones and Bone Tissue

The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
Bone Formation by Intramembranous Ossification01:29

Bone Formation by Intramembranous Ossification

Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
The process begins when mesenchymal cells in the embryonic skeleton gather together and differentiate into osteogenic cells, which then develop into...
Growth of Cartilage and Bone Tissue01:27

Growth of Cartilage and Bone Tissue

Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during bone...
Changes in the Appendicular Skeleton with Age01:09

Changes in the Appendicular Skeleton with Age

The upper and lower limb initially develops as a small bulge called a limb bud, which appears on the lateral side of the early embryo. The upper limb bud appears near the end of the fourth week of development, with the lower limb bud appearing shortly after.
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Updated: Jun 13, 2026

Exploring Independent Effects of Follicle-Stimulating Hormone In Vivo in a Mouse Model
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Exploring Independent Effects of Follicle-Stimulating Hormone In Vivo in a Mouse Model

Published on: August 11, 2023

Commentary-FSH and bone 2010: evolving evidence.

Jameel Iqbal1, Li Sun, Mone Zaidi

  • 1The Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, New York, USA.

European Journal of Endocrinology
|May 8, 2010
PubMed
Summary
This summary is machine-generated.

Elevated follicle-stimulating hormone (FSH) directly stimulates bone resorption, contributing to bone loss during menopause. This pituitary-bone axis effect is independent of estrogen and significant in perimenopause.

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Area of Science:

  • Endocrinology
  • Bone Biology
  • Reproductive Medicine

Background:

  • Menopausal bone loss is traditionally linked to decreased estrogen.
  • Significant bone loss occurs pre-menopause when estrogen levels are stable but FSH is elevated.
  • Existing research suggests a potential role for FSH in bone metabolism.

Purpose of the Study:

  • To investigate the direct role of FSH in stimulating bone resorption.
  • To explore the pituitary-bone axis in the context of menopausal bone loss.
  • To determine FSH's contribution to bone loss during the menopausal transition.

Main Methods:

  • Cell-based assays to examine FSH effects on osteoclasts.
  • Mouse genetic studies to elucidate FSH signaling pathways.
  • Analysis of human genetic polymorphisms (rs6166) associated with bone mass.

Main Results:

  • FSH directly stimulates osteoclast-mediated bone resorption.
  • This effect is independent of estrogen levels.
  • An 'activating' FSH polymorphism (rs6166) is linked to low bone mass and high bone turnover in humans.

Conclusions:

  • Elevated FSH, via a pituitary-bone axis, contributes significantly to bone loss during the menopausal transition, particularly in late perimenopause.
  • FSH signaling plays a primary role in regulating human bone mass and remodeling.
  • Targeting FSH may offer new therapeutic strategies for preventing menopausal bone loss.