The final bow: many ways to die
Cell or tissue death follows irreversible injury due to a variety of etiologies. Apoptosis, morphologically a ‘falling out’ of a single cell from its surrounding tissues, is programmed and tightly regulated. In both physiological and pathological situations, its significance lies in leaving surrounding tissues undisturbed with absence of an inflammatory response: scavengers (macrophages) quietly removing the cell debris. Necrosis, however, entails significant loss of tissue volume, evokes an inflammatory response, manifests with local and/or systemic clinical symptoms and signs and, eventually, affects tissue structure (clinically and on imaging) and function (altered hematologic, biochemical and immunologic parameters). Macroscopic appearances range from the black discoloration of gangrene – dry/wet/gas; the fluctuating consistency of an abscess accompanied by the classical signs of inflammation; cheesy transformation of caseous necrosis etc. Microscopic examination of affected tissues may show single cell drop out or cell fragments (apoptosis) versus the ghost outlines of coagulative necrosis, collections of neutrophils with no intact cells in liquefactive necrosis or the caseating centers of necrosis in granulomas due to mycobacterial and some fungal infections.
Insights and Impact
- The physician’s alertness and rapid response rests on fundamental pathological insights of limited opportunities during progression from reversible to irreversible cell injury
- Vulnerability of an organ to hypoxia, the criticality of its function, and time-lapse since the etiological insult, constitute a triad – formulaic to intervention
- The brain, heart and kidneys stand out as key examples where timely response delimits damage, reduces morbidity and avoids mortality
- The most visible clinical sign of necrosis is the ominous blackening of an anatomical region due to gangrene, most often in an extremity
- The circumstances triggering apoptotic death need insightful expectant diagnosis since it can only be visualized on microscopy
- Necrosis, in all its morphological variants, can be identified clinically and/or corroborated by investigation modalities
Rhythm ’n rhyme
Ashes to ashes…
Long before humans die, body and soul
Death of cells and tissues has been ongoing: ‘tis no hyperbole;
Apoptosis: a programmed single cell death, is quiet as a mouse
Necrosis: demise of tissues en masse, shakes up the organ house;
Apoptosis is mediated by intrinsic or extrinsic pathways
Organ development, viruses and radiation the etiological mainstays.
Intracellular caspases cascade the process to inevitable solitary cell demise
Surrounding tissues left untouched, no inflammatory response: ‘tis no surprise
Necrosis does the full Monty, catastrophic the extent of damage
Provokes an inflammatory response, cytokines are on the rampage.
Ischemia, thermal injury, cause coagulative necrosis
Liquefactive when in the brain or when a bacterial infection causes an abscess;
Be warned when you observe your diabetic patient’s toe turning black
Gangrene is the spot diagnosis: if neglected the limb may need a hack;
Dry-mummified due to peripheral ischemia, Wet-fluctuant with superadded infection
Beware if it is crepitant, clostridial gas gangrene is likely the dreaded affliction.
Deep Dive
A. The intrinsic and extrinsic pathways of apoptosis (Fig. 2 – referenced article)
Acknowledgement:
http://Creative Commons Attribution-NonCommercial 4.0 International
Cancer, Natural Products and Nanodrug Delivery Systems – Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/figure/The-intrinsic-and-extrinsic-pathways-of-apoptosis-35_fig1_342829967 [accessed 28 Dec 2025]
Q. 1. Recall three etiologies of cell damage that trigger apoptosis
Q. 2. Why does prolonged UV exposure trigger apoptosis in skin cells?
B. Clinical appearances of gangrene
Acknowledgement:
https://www.slideshare.net/slideshow/gangrene-240083697/240083697
Q. In addition to the types of gangrene displayed in the image above, which unique types of gangrene affect scrotal skin and postoperative wounds?
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