Related Experiment Video

Updated: Jul 22, 2026

Detection and Analysis of DNA Damage in Mouse Skeletal Muscle In Situ Using the TUNEL Method
09:54

Detection and Analysis of DNA Damage in Mouse Skeletal Muscle In Situ Using the TUNEL Method

Published on: December 16, 2014

Microdamage and apoptosis

Brendon Noble1

  • 1Scottish Mechanotransduction Consortium, University of Edinburgh Medical School, Edinburgh, UK. Brendon.Noble@ed.ac.uk

European Journal of Morphology
|August 27, 2005
PubMed

Insights

Bone microdamage repair relies on unknown signals. Osteocytes may sense and target damage, with their apoptosis potentially playing a key role in this process, which declines with age and disease.

Area of Science:

  • Bone biology and mechanobiology
  • Cellular signaling in skeletal health
  • Osteocyte function and apoptosis

Background:

  • Healthy bone self-repairs microdamage through targeted removal and regeneration.
  • This repair process necessitates specific signaling molecules, the identity of which remains unknown.
  • Impairment of this targeting mechanism is observed in aging and various bone diseases.

Purpose of the Study:

  • To investigate the potential role of matrix-bound osteocytes in sensing and targeting bone microdamage.
  • To review current knowledge on osteocyte apoptosis at sites of microdamage.
  • To discuss the physiological significance of osteocyte apoptosis in microdamage repair.

Main Methods:

  • Literature review of osteocyte biology and microdamage response.
  • Analysis of existing research on apoptosis in cellular systems.
  • Discussion of potential signaling mechanisms involving osteocytes.

Main Results:

  • Osteocytes, embedded within the bone matrix, are strategically positioned to detect mechanical stress and microdamage.
  • Apoptotic cell death of osteocytes is frequently observed at sites of microdamage.
  • The extent and significance of osteocyte apoptosis in targeting and initiating repair are under investigation.

Conclusions:

  • Osteocytes are likely key players in sensing and targeting bone microdamage.
  • Osteocyte apoptosis may serve as a critical signal or component in the bone repair cascade.
  • Understanding osteocyte-mediated signaling is crucial for addressing age-related bone loss and disease.

More Related Videos

Application of Laser Micro-irradiation for Examination of Single and Double Strand Break Repair in Mammalian Cells08:18

Application of Laser Micro-irradiation for Examination of Single and Double Strand Break Repair in Mammalian Cells

Published on: September 5, 2017

Detection and Isolation of Apoptotic Bodies to High Purity12:17

Detection and Isolation of Apoptotic Bodies to High Purity

Published on: August 12, 2018

Related Concept Videos

Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...