Healing of Mucosal Surfaces

The cells of mucosa have very good regeneration and are normally being lost and replaced continuously, e.g. mucosa of alimentary tract, respiratory tract, urinary tract, uterine endometrium, etc. This occurs by proliferation from margins, migration, multilaye-ring and differentiation of epithelial cells in the same way as in the epidermal cells in healing of skin wounds.

Healing of Solid Epithelial Organs

Following gross tissue damage to organs like kidney, liver and thyroid, the replacement is by fibrous scar, e.g. in chronic pyelonephritis and cirrhosis of liver. However, in parenchymal cell damage with intact basement membrane or intact supporting stromal tissue, regeneration may occur. For example, in tubular necrosis of kidney with intact basement membrane, proliferation and slow migration of tubular epithelial cells may occur to form renal tubules; in viral hepatitis if part of the liver lobule is damaged with intact stromal network, proliferation of hepatocytes may result in restoration of liver lobule.

ADAPTATION

Cells as adaptable units. Cells are constantly exposed to changes in their environment. The conditions to which cells are exposed are subject to constant change as a result of normal physiological processes, and also because of changes in the external environment, including the effects of medical treatment. If cells were static and rigid systems, these changes in the cellular environment would profoundly affect function of tissues, but there are homeostatic mechanisms which allow cells and tissues to cope with such stresses. Cells adapt to acceptable changes in their environment by modifying metabolism or growth pattern.

To maintain normal function, cells have a physiological ability to adapt to acceptable environmental changes. Many of these modifications are physiological metabolic adaptations, and represent fine regulation of metabolic function at a biochemical level.

Other cell adaptations to environmental change are (physiological structural adaptations) caused by a change in the normal pattern of growth and accompanied by easily detectable structural changes.

The cell stress response to injury. Damaged cells produce proteins which protect them from damage. In response to some pathological stimuli, cells exhibit a series of metabolic changes known as the cell stress response, which is an important basic cellular mechanism that enables cells to survive environmental insults. Stressed cells turn down the genes coding for normal structural proteins (housekeeping genes) and show high levels of expression of genes coding for a set of proteins which have cell-organizing and protective functions (cell stress genes). Many of the cell stress proteins were originally described in response to experimental heat shock, hence a major group is termed the heat shock proteins (HSPs). The general terms «heat shock protein» and «cell stress protein» are synonymous. Cell stress proteins are vital for cell viability. The stress proteins are expressed at low levels in normal cells, where they have important roles, but levels increase following exposure to damaging stimuli. Their increased production in a cell

stress response provides the extra stress proteins needed in pathological conditions.

In certain cells which undergo chronic stress, permanent aggregates of abnormal cell constituents and ubiquitin form visible masses known as inclusion bodies within the cytoplasm. One example of this phenomenon is when liver cells are chronically exposed to alcohol and form masses of the intermediate filament cytokeratin and ubiquitin, visible as pink-stained inclusion bodies. These are eponymously termed Mallory's hyaline. Another example is the Lewy body in nerve cells. Production of the cell stress proteins following exposure to a damaging stimulus is a rapid response that minimizes cell damage and ensures cell viability. Cell stress proteins can only protect against certain levels of damage, with more severe stimuli leading to cell degeneration or death.