Table of contents :

  • degenerations
  • cell senescence
  • cell death
  • necrosis
  • gangrene

  • type of cell death
    morphological changes
    biochemical features
    common detection methods
    cell membrane
    apoptosis or active (programmed) cell death (ACD / PCD) chromatin condensation; nuclear fragmentation; DNA laddering blebbing  fragmentation (formation of apoptotic bodies) Caspase-dependent electron microscopy; TUNEL staining; annexin staining; caspase-activity assays; DNA-fragmentation assays; detection of increased number of cells in subG1/G0; detection of changes in mitochondrial membrane potential
    Autophagy partial chromatin condensation; no DNA laddering blebbing increased number of autophagic vesicles caspase-independent; increased lysosomal activity electron microscopy; protein-degradation assays; assays for marker-protein translocation to autophagic membranes; monodansylcadaverine (MDC) staining
    mitotic catastrophe multiple micronuclei; nuclear fragmentation
    caspase-independent (at early stage) abnormal CDK1/cyclin B activation electron microscopy; assays for mitotic markers (mitotic phosphoprotein 2 (MPM2)); TUNEL staining
    necrosis clumping and random degradation of nuclear DNA swelling; rupture increased vacuolation; organelle degeneration; mitochondrial swelling
    electron microscopy; nuclear staining (usually negative); detection of inflammation and damage in surrounding tissues
    cell senescence distinct heterochromatic structure (senescence-associated heterochromatic foci)
    flattening and increased granularity senescence-associated b-galactosidase (SA-b-gal) activity electron microscopy; SA-b-gal staining; growth-arrest assays; assays for increased p53, INK4A and ARF levels (usually increased); assays for RB phosphorylation (usually hypophosphorylated); assays for MMP activity (usually upregulated)
  • peliosis is a pathological entity characterized by the gross appearance of multiple cyst-like, blood-filled cavities within parenchymatous organs. Peliosis has been related to several underlying debilitating illnesses such as tuberculosis, hematological malignancies, the acquired immunodeficiency syndrome (AIDS), and post-transplant immunodeficiency, as well as intravenous drug abuse, chronic alcoholism, and in conjunction with the intake of oral contraceptives or steroids. The classical pathoanatomical concept is based upon the opinion that peliosis exclusively develops in organs belonging to the mononuclear phagocytic system (liver, spleen, bone marrow, and lymph nodes). However, a paucity of studies indicates that other organs such as lungs, parathyroid glands, and kidneys may be affected too. Concerning the underlying pathogenetic mechanisms of onset and maintenance of peliosis, the morphological data obtained by different investigators suggest that there is more than one path of formal pathogenesis (e.g., congenital malformation of vessels manifesting under altered local intravascular pressure conditions, acquired vascular disorder triggered by toxic noxae, active proliferation of vessels corresponding to the benign end on the spectrum of neoplastic vascular lesions).
  • in the liver, at gross inspection, the peliotic lesions give the cut sections a "swiss cheese" appearance. Microscopically, 2 different types of peliosis can be distinguished in the liver :
  • parenchymal peliosis consisting of irregular cavities that are neither lined by sinusoidal cells nor by fibrous tissue
  • phlebectatic peliosis characterized by regular, spherical cavities lined by endothelium and/or fibrosis.
  • One of the differential diagnoses that most closely resembles peliosis hepatis is secondary hepatic congestion due to veno-occlusive disease or the Budd-Chiari syndrome.
  • in the spleen, the peliotic lesions may be arranged sporadically, disseminated, or in clusters in an uneven distribution pattern. Histologically, the cavities show frequently well-demarcated margins that may appear focally lined by sinusoidal endothelium, or totally lack a clear cell lining. Differential diagnoses are hemangiomas and involvement of the spleen in hairy-cell leukaemia. Since the disease may culminate in spontaneous rupture of the affected organ and thus may mimic a violent death at autopsy, peliosis is far more than just another morphological curiosity. Awareness of peliosis at autopsy as well as an appreciation for the histopathological changes in less characteristic or advanced cases may become an important issue for both the forensic and clinical pathologistref

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