Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

3.6K
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...
3.6K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

6.1K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.1K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.2K
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...
6.2K
Necrosis01:16

Necrosis

4.2K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
4.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Mechanochemically Coupled Multidimensional Modulation of Calcium Overload.

ACS nano·2026
Same author

Mesoporous Catalytic-Adsorptive Nanoregulator Orchestrates Biofilm eDNA/LPS Disassembly and TLR9/TLR4 Immune Reprogramming to Resolve Diabetic Foot Infections.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Correction: Deficient or R273H and R248W mutations of p53 promote chemoresistance to 5-FU via TCF21/CD44 axis-mediated enhanced stemness in colorectal carcinoma.

Frontiers in cell and developmental biology·2026
Same author

Single-Cell Analysis Identifies LYPD6B as a Tumor-Intrinsic Candidate Associated With Immunotherapy Nonresponse in Breast Cancer.

Thoracic cancer·2026
Same author

Screening of polyphenolic cathepsin B inhibitors and proteomic insights into muscle protection in grass carp during chilled storage.

Food chemistry·2026
Same author

Seed coating transfers neonicotinoid risk to pollinators more efficiently than conventional sprays: A field study in rice production.

Journal of hazardous materials·2026
Same journal

Structural Validity and Factorial Analysis of the Brazilian Oral Health Impact Profile for Temporomandibular Disorders Instrument.

Oral diseases·2026
Same journal

Effects of Pistacia lentiscus Leaf-Twig and Resin (Mastic) Oils on Salivary Flow in Healthy Individuals.

Oral diseases·2026
Same journal

Oral Delivery of Bioencapsulated CTB-Pro-IGF-1 Enhances Bone Regeneration in a Pre-Clinical Rat Model of Jaw Osteoradionecrosis.

Oral diseases·2026
Same journal

Trends in Stage and Age at Diagnosis of Oral Squamous Cell Carcinoma Over Time: A Systematic Review and Meta-Analysis.

Oral diseases·2026
Same journal

Ion Channel Dysfunction and Therapeutic Targeting in Salivary Gland Disorders.

Oral diseases·2026
Same journal

Authors' Reply "Synchronous Soft-Tissue Lesions in the Oral Cavity in an Adolescent".

Oral diseases·2026
See all related articles

Related Experiment Video

Updated: May 31, 2025

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
06:12

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

1.7K

Programmed Cell Death Tunes Periodontitis.

Yuejiao Xin1,2, Yixiang Wang3

  • 1Department of Periodontics, Tianjin Stomatological Hospital, School of Medicine, Nankai University, Tianjin, China.

Oral Diseases
|January 23, 2025
PubMed
Summary
This summary is machine-generated.

Programmed cell death pathways are crucial in periodontitis, influencing immune responses and disease progression. Understanding these processes offers potential for new therapeutic strategies against this complex infection.

Keywords:
apoptosisautophagynecroptosisperiodontitisprogrammed cell deathpyroptosis

More Related Videos

Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
06:14

Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model

Published on: February 17, 2023

3.7K
Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
07:15

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

11.3K

Related Experiment Videos

Last Updated: May 31, 2025

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
06:12

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

1.7K
Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
06:14

Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model

Published on: February 17, 2023

3.7K
Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
07:15

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

11.3K

Area of Science:

  • Immunology
  • Cell Biology
  • Periodontal Disease Research

Background:

  • Programmed cell death (PCD) is essential for multicellular organism homeostasis.
  • PCD pathways are critical in balancing cell survival and death during infection and disease.
  • Periodontitis involves complex interactions between microbial virulence factors and host immune responses.

Purpose of the Study:

  • To review current knowledge on programmed cell death processes.
  • To elucidate the roles of programmed cell death in the immunoregulation of periodontitis.

Main Methods:

  • A comprehensive literature search was conducted in PubMed, Medline, and Scopus databases.
  • A narrative review methodology was employed.
  • The review focused on programmed cell death pathways implicated in periodontal infection.

Main Results:

  • Programmed cell death is central to managing cell death and survival in pathological conditions and infections.
  • Periodontitis pathogenesis is influenced by diverse programmed cell death mechanisms, which can have opposing or combinatorial effects.
  • Host immune responses in periodontitis are tightly regulated and interact with microbial factors.

Conclusions:

  • The interplay and coordination of various programmed cell death pathways are fundamental to periodontitis pathophysiology.
  • Further research into the specific roles and mechanisms of programmed cell death in periodontitis may reveal novel therapeutic targets.