Vascular Cellular Repair and inflammation response

Sequence Of Events for Vascular Cellular Repair and the Inflammation Response

1. A break in the skin occurs
2. Bacterial reproduction increases
3. Macrophages engulf bacteria
4. Macrophages secrete cytokines
5. Activated mast cells secrete histamine
6. Histamine and cytokines increase dilation of blood vessels
7. White blood cells (WBCs) adhere to capillary lining (pavementing)
8. WBCs migrate to injured site via endothelial cellular gaps via diapedis movement
9. Monocytes turn into macrophages
10. Macrophages and neutrophils engulf pathogens (phagocytosis)
11. Red Blood Cells increase in concentration causing redness and head
12. An increased amount of fluid migrates to the area causing swelling and pain.
13. Tissue repair commences and systemic responses may be evident e.g. fever

What is involved in the tissue repair response?

Resolution – the toxin is neutralized, oedema decreases, capillary permeability decreases and vasoconstriction occurs

Regeneration & replacement – proliferation of identical cells. Dependent on cells ability to regenerate (Labile, Stable & Permanent/Fixed)

Labile cells - Continuous diversion and replication, infused by growth factors

Stable cells – stop dividing when growth ceases, however, can regenerate if given appropriate stimulus e.g. liver cells

Permanent/fixed cells – cannot undergo mitotic division e.g. nerve cells. If destroyed they are replaced with fibrous scar tissue.

Connective tissue repair – Formation of scar tissue, proliferation from surrounding areas extending into the damaged tissue. Primary and secondary intention. Primary (outside-in), secondary (inside-out)

Primary – faster and no scar tissue formed.

Wound healing has 3 phases:

1. Inflammation
2. Proliferation
3. Remodelling

Chronic Inflammation

Acute infections are self-limiting and controlled by host defences. Chronic inflammation is self-perpetuating and may last weeks, months etc. There is an increased chance of scarring and tissue destruction. Chronic inflammation is typically evoked by irritants e.g. talc, asbestos, bacteria and fungi. Acute inflammation may progress to chronic inflammation.

 What is the difference between acute and chronic inflammation?

Acute Inflammation	Chronic Inflammation
Exudate present	Cellular response (fibroblasts)
Neutrophils are the predominant cells	Lymphocytes, plasma cells, macrophages and fibroblasts are the predominant cells present. When plasma cells and lymphocytes are identified at the same time, this indicates repair and inflammation are occurring at the same time.
Swelling and interstitial fluid present including proteins and white blood cells	Due to laying down of fibrous tissue by fibroblasts that give rise to granulomas.

Additional information about acute and chronic inflammation can be found here 

What is a Granuloma?

Firstly, a granuloma is not the same as granulation tissue. A granuloma lesion is approximately 1-2mm and caused by chronic inflammation. Increased macrophages and lymphocytes are at the site. These macrophages are modified cells resembling epithelial cells (also called epitheliod cells). 

A Granuloma is formed to ward off toxins from the rest of the body. Poorly digested, not easily controlled. Epitheliod cells clump in a mass (granuloma) forming a large multinucleated giant cell that attempts to surround the toxin. A dense membrane of connecting tissue encapsulated and a lesion is formed.

Tuberculosis is associated with granulomas M.Tuberculosis is resistant to phagocytes. Calcium may then be deposited into granuloma (tubercle) then casseous necrosis occurs in the centre.