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Related Concept Videos

Bone Remodeling01:40

Bone Remodeling

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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Osteoclasts in Bone Remodeling01:31

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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...
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Fractures: Bone Repair01:27

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Treatment for a fracture is based on the type of break, the bone affected, and the patient's age.
Minor fractures with no bone displacement are treated by immobilizing the fractured bone using a cast or splint. However, in the case of fractures with displaced bones, the broken bones are repositioned before immobilization to ensure successful healing without deformation and loss of function. The realignment of fractured bone ends is performed through a process called reduction. If the...
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Bone Disorders01:29

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
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Related Experiment Video

Updated: Feb 18, 2026

Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model
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Improved Methodology for Studying Postnatal Osteogenesis via Intramembranous Ossification in a Murine Bone Marrow Injury Model

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[Aberrant bone remodeling during sepsis.]

Asuka Terashima1

  • 1Department of Osteoimmunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Japan.

Clinical Calcium
|November 28, 2017
PubMed
Summary

Sepsis causes immune deficiency by reducing lymphocytes. Osteoblasts play a key role in regulating lymphocyte production during sepsis, and their loss impairs immune function.

Area of Science:

  • Immunology
  • Hematology
  • Bone Biology

Background:

  • Sepsis, a severe bacterial infection, triggers a systemic inflammatory response.
  • While early sepsis treatment improves survival, immunosuppression leading to secondary infections remains a challenge.
  • Lymphopenia, a reduction in lymphocytes, is a known cause of sepsis-induced immune dysfunction, but mechanisms are unclear.

Purpose of the Study:

  • To investigate the mechanisms underlying sepsis-induced lymphopenia and immunosuppression.
  • To elucidate the role of osteoblasts in regulating lymphopoiesis during systemic inflammation.

Main Methods:

  • Induction of acute inflammation to model sepsis.
  • Quantification of peripheral lymphocytes and bone marrow common lymphoid progenitors (CLPs).

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  • Assessment of osteoblast numbers and function.
  • Generation of osteoblast-specific IL-7 knockout mice to study osteoblast-lymphopoiesis interactions.

    • Main Results:

    • Acute inflammation led to a significant reduction in peripheral lymphocytes and bone marrow CLPs.
    • This reduction in lymphocytes correlated with a dramatic decrease in osteoblast numbers.
    • Osteoblast-specific deletion of IL-7 confirmed the critical role of osteoblasts in maintaining lymphopoiesis during systemic inflammation.
    • Loss of osteoblasts during sepsis disrupted lymphocyte homeostasis, causing immunodeficiency.

    Conclusions:

    • Osteoblasts are crucial regulators of lymphopoiesis, particularly during systemic inflammation like sepsis.
    • The acute loss of osteoblasts in sepsis contributes to lymphocyte reduction and subsequent immunodeficiency.
    • Targeting osteoblast function may offer a novel therapeutic strategy to combat sepsis-induced immunosuppression.