Balzhan Beibitkyzy
Scientific supervisor: Beysenova Aizhan Zhumagazievna- candidate of biological sciences, professor
Introduction
Every day, millions of cells in the human body die, and this is completely normal. Cell death is not only a destructive event; in many cases it is necessary for the organism to stay healthy. Without controlled cell death, the body would accumulate damaged cells, organ structures would not form properly, and the risk of cancer would dramatically increase.
In medicine, the two main types of cell death are apoptosis and necrosis. Although both end in the death of a cell, they happen through very different mechanisms and have very different consequences. Understanding these differences is important for medical students, because both processes appear in inflammation, cancer, infections, developmental biology, and ischemic conditions such as stroke and heart attack.
This article explains apoptosis and necrosis in a clear, human-like way, suitable for a first-year medical cytology course.
1. The Essential Difference Between Apoptosis and Necrosis
The main difference is control versus loss of control.
1.1 Apoptosis: controlled cell death
Apoptosis is a regulated, genetically programmed form of cell death. The cell prepares itself to die, activates internal enzymes, and dismantles itself step by step. This process requires energy (ATP) and does not harm neighboring cells.
Apoptosis is important for:
- normal embryonic development
- the immune system
- removing cells with DNA damage
- preventing tumor formation
- maintaining tissue homeostasis
Because apoptosis is neat and quiet, the body does not respond with inflammation.
1.2 Necrosis: uncontrolled cell destruction
Necrosis occurs when a cell is exposed to something it cannot survive. This may include:
- toxins or chemicals
- infections
- extreme lack of oxygen
- physical trauma
- very high or very low temperatures
Necrosis is unplanned. The cell swells, bursts, and releases its contents into the surrounding tissue. This causes inflammation, pain, and additional tissue damage.
2. Molecular Mechanisms of Cell Death
2.1 How apoptosis works
There are two main pathways:
a) Intrinsic (mitochondrial) pathway
Triggered internally by:
- DNA damage
- oxidative stress
- lack of growth factors
Mitochondria release cytochrome c, which activates caspases — enzymes that break down the cell in a precise manner.
b) Extrinsic (death receptor) pathway
Triggered externally by:
- Fas receptor
- TNF receptors
- immune signaling
This also activates caspases but starts at the cell membrane.
Both pathways converge into the same controlled execution phase.
2.2 How necrosis works
Necrosis does not use caspases.
It happens due to:
- severe ATP depletion
- disruption of the plasma membrane
- uncontrolled ion influx
- osmotic swelling
- membrane rupture
Because contents spill out, necrosis always causes inflammation.
3. Morphological Features Under the Microscope
3.1 Apoptosis
Apoptotic cells show:
- cell shrinkage
- dark, condensed chromatin (pyknosis)
- nuclear fragmentation (karyorrhexis)
- intact cell membrane
- formation of apoptotic bodies
Macrophages quickly remove these fragments, so apoptosis is usually invisible at the tissue level.
3.2 Necrosis
Necrotic cells show:
- swelling
- disrupted membranes
- vacuolated cytoplasm
- faded or dissolved nuclei (karyolysis)
- surrounding inflammation
Necrosis often appears as large areas of damaged tissue rather than isolated cells.
4. Biological and Medical Importance of Each Process
4.1 Why apoptosis is necessary
Apoptosis is essential for:
- embryonic formation (e.g., separating fingers)
- removing infected or mutated cells
- preventing autoimmune diseases
- eliminating cells with irreparable DNA damage
If apoptosis is reduced or defective, conditions such as cancer, chronic infections, and autoimmune diseases may develop.
4.2 Why necrosis is medically important
Necrosis is common in many acute conditions, including:
- myocardial infarction
- stroke
- severe infections
- burns
- toxic injuries
Because necrosis causes inflammation, it often leads to pain, swelling, and organ dysfunction.
5. Clinical Applications for Medical Students
5.1 Necrosis in diagnosis
Blood tests often detect necrosis. For example:
- troponins increase in heart muscle necrosis
- ALT/AST rise in liver necrosis
- amylase/lipase rise in pancreatic necrosis
Understanding necrosis helps interpret lab results accurately.
5.2 Apoptosis in therapy
Many cancer treatments, such as chemotherapy and radiation therapy, work by triggering apoptosis in tumor cells.
Tumors with defective apoptosis (for example, those with a mutated p53 gene) become:
- more aggressive
- harder to treat
- more resistant to therapy
This makes apoptosis a critical topic for future physicians.
Conclusion
Although both apoptosis and necrosis end in the death of a cell, they have opposite roles in the body. Apoptosis is a clean, controlled, beneficial process essential for development and protection against disease. Necrosis, by contrast, is uncontrolled and usually harmful, occurring in severe injuries and pathological states.
For first-year medical students, understanding these differences helps build a strong foundation for future studies in pathology, oncology, pharmacology, and clinical medicine. Cytology provides the tools to recognize these processes under the microscope and understand their importance in health and disease.
References
(Все реальные и подходят для студенческой работы)
- Alberts, B., Johnson, A., Lewis, J., et al. Molecular Biology of the Cell. 6th Edition. Garland Science, 2015.
- Kerr, J. F. R., Wyllie, A. H., & Currie, A. R. “Apoptosis: A Basic Biological Phenomenon with Wide-ranging Implications in Tissue Kinetics.” British Journal of Cancer, 1972.
- Elmore, S. “Apoptosis: A Review of Programmed Cell Death.” Toxicologic Pathology, 2007.
- Kumar, V., Abbas, A. K., Aster, J. C. Robbins & Cotran Pathologic Basis of Disease. 10th Edition. Elsevier, 2020.
- Majno, G., & Joris, I. “Apoptosis, Oncosis, and Necrosis.” The American Journal of Pathology, 1995.
- Reed, J. C. “Mechanisms of Apoptosis.” The American Journal of Pathology, 2000.
- Fulda, S., & Debatin, K. M. “Extrinsic Versus Intrinsic Apoptosis Pathways in Cancer Therapy.” Oncogene, 2006.