Any injury that causes the cells to die will elicit and inflammatory response. This is to remove the debris of the dead cells and the source of the injury. Inflammation can be acute or chronic, but whatever type, phagocytic cells and blood proteins move to the area of infection. The response is dependant on both vasoactive and chemotactic messengers from the site of injury, and these cells cause the arrival of inflammatory cells at the injury site.
Acute inflammation works to remove any external invader and any narcotic cellular debris. To do this phagocytes are attracted to the area by parts of the clotting components. For example vasodilation and release of chemotaxis messengers from the cells and blood plasma. The outcome of acute inflammation depends on the type and persistence of the injury the extent of the damage and how the specialised cells on the injury site proliferate. In chronic inflammation, the causative agent will continue for a long time and continue to cause injury.
Mast cells release histamine which causes vasodilation, increased plasma permeability of the vessels to phagocytic cells and fluid. This causes the injury site to be flooded with phagocytic cells, fluids and plasma proteins, this is called inflammatory exudate.
Signs of inflammation
- Redness – dilation of the local blood vessels
- Heat – from increased blood flow
- Swelling – from the build-up of fluids and plasma proteins and loss of function due to tissue swelling.
The fluid and plasma proteins work by diluting any substances that may cause injury before they are drained into the hepatic system. Immunoglobulins and part of the complement cascade help to neutralise the microorganism. Other proteins like fibrinogens are converted int insoluble for which forms a mesh at the injury site.
The mesh plugs the wound and physically protecting it from infections. The first cells to arrive at the site are the neutrophils that phagocytose necrotic cellular debris, by releasing phagocytic enzymes from the lysosomes. When they have used, the lysosomes enzymes die and become part of the debris.
The mast cells arrive at the area, monocytes are tuned into macrophages when they activated. They can regenerate their phagocytic enzymes hence they digest the narcotic cellular debris. The lymphocytes may be part of the specific or non-specific immune mechanism or may have been freed from the tissue that was broken down by injury.
Repair is done through with regeneration, this is where old tissue is replaced by the same type cells. And replacement by connective tissue. Regeneration of tissue can only happen when there are reserve cells at the site of injury that are able to go through mitosis. there usually are three groups of cells
- Labile cells – these are cells that generally proliferate throughout the lifespan replacing dead or dying cells that die through normal physiological means. For example the epithelial at the surface of the skin.
- Stable cells – reiterate but usually don’t because they have long survival time, for example, the cells of the glands, liver cells and the cells of the kidney collecting tubules.
- Permanent cells – these are neutrons and cardiac muscles cells, if a neuron dies, it is lost forever. But the axons can reiterate after an injury. Cardiac muscle cells die because of deprived oxygen as seen in heart attacks. Repair depends on the existing framework being presented and if there is adequate blood supply.
Angiogenesis is the formation of new blood vessels, that bud and sprout from pre-existing blood vessels. They form several branches which eventually grow and form capillary beds. They will subsequently form capillary beds and venules. Growth factors are usually involved during angiogenesis.
Mechanism of Healing
Normal growth in cells is controlled by both growth factors and inhibitors. The most important are the factors that recruit quiescent cells to mitosis. These growth factors are called.
- Epidermal GF- mutagenic for epidermal cells and fibroblasts, it is involved in collagen formation and therefore speeds up the healing process, in the skin and the cells that line the GI.
- PDGE – growth factors comes from platelets but also from activated macrophages, endothelium, smooth muscles cells and tumour cells. It causes the migration and proliferation of fibroblasts, smooth muscle cells and the monocytes.
- FGF – comes from the fibroblasts, causes fibroblasts proliferation and new vascular growth. There are two types, we have the beta FGF that are found in most of the organs and secreted by the activated macrophages. The second is Alpha FGF which is located in the neural tissue.
Darby, I. A., Laverdet, B., Bonté, F., & Desmoulière, A. (2014). Fibroblasts and myofibroblasts in wound healing. Clinical, cosmetic and investigational dermatology, 7, 301.
Shabbir, A., Cox, A., Rodriguez-Menocal, L., Salgado, M., & Badiavas, E. V. (2015). Mesenchymal stem cell exosomes induce proliferation and migration of normal and chronic wound fibroblasts, and enhance angiogenesis in vitro. Stem cells and development, 24(14), 1635-1647.
Portou, M. J., Baker, D., Abraham, D., & Tsui, J. (2015). The innate immune system, toll-like receptors and dermal wound healing: a review. Vascular pharmacology, 71, 31-36.
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