Chronic inflammation.

With injury of a short duration, an acute, brief inflammatory reaction occurs. with prolonged tissue injury, or a persistent infection, chronic inflammation occurs. the important difference is that chronic inflammation results in the production of vascular granulation tissue which matures into fibrous tissue. the changes are proliferative in contrast to the exudative changes of acute inflammation. acute inflammation may terminate in fibrosis and some proliferation does occur. when the acute stage fails to resolve, the exudative and proliferative phases are often associated together. the more chronic the inflammation, the more pronounced the proliferative change and the greater the degree of fibrous scarring ultimately.

causes and types of chronic inflammation.

1 chronic with acute onset

the best example is bacterial infection, the infection is usually eliminated and the tissues return to normal, there may be some scarring. in some cases, a low grade infection may persist and may progress to the chronic stage. the bacterial infection may flare up from time to time and cause abscesses.

2 chronic infection with insidious onset.

caused by agents which cause low grade but persistent tissue injury, four sub groups:

a particulate matter which stimulates fibrogenesis. reason unknown but may be due to the release of lyposomal enzymes.

b microbial infections e.g. bacteria/fungal.

c hypersensitivity infections e.g. contact dermatitis.

d unknown agents e.g. ulcerative colitis.

in chronic inflammation, the arteries of the affected area show proliferation of the tunica intima. this is inflammatory endarteritis and may seriously diminish the lumen of the vessels leading to degeneration and fibrous replacement of specialised tissues, ischaemic necrosis and delayed healing. may affect veins = endophlebitis.

the termination of inflammation.

four options exist:

1 resolution complete restoration of function, no scarring, occurs if only tissue trauma is minimal.

2 fibrosis degree of residual scarring varies. fibrosis may occur from the organisation of fibrin rich exudate. you will be involved frequently in dealing with this accumulation of fibrous tissue. almost all major injuries result in scar tissue formation e.g. ligament tears, muscle tears.

3 suppuration this is usually due to invasion by pus forming bacteria (pyogenic) and is a mixture of liquefied tissue, bacteria, inflammatory exudate and other particles.

4 necrosis = tissue death e.g. gangrene.

tissue repair

there are two processes: | | | |

primary union & secondary union. (first intention) (second intention)

primary.

after minimal tissue loss with no significant infection.

e.g. scalpel incision

wound edges approximated and the small space fills with

blood clot.

0-24hrs- neutrophils arrive

day 3 - neurtophil/monocyte infiltration, granulation tissue

invades incisional space. collage present at margins.

epithelial cells proliferate and thicken.

day 5 space completely filled by granulation tissue. collagen bridges across area. angiogenesis occurs. epidermis recovers iyts normal thickness and cell differentiation 14 days collagen & fibroblast activity continues. by 1 month, no inflammatory products left. tensile strength of scar increases over several months

secondary when tissue loss is extensive e.g. pressure sore, infarction. the repair process is more complicated here. large defects must be filled. there is extensive granulation tissue formed, and more debris removed. scar contraction may occur. the scar may contract 5-10% of its original length.

summary of wound healing types

first intention second intention

1 scab formation2 granulation tissue containing macrophages, new capillaries and fibroblasts.3 fibrous union4 wound contraction

factors affecting healing.

whilst pathologists talk about timescales in the healing and repair process, you should understand that healing is subject to individual variations. it is also affected by:

age young tissues heal more quickly than old ones.

drugs certain drugs e.g. steroids, delay wound healing. some drugs used in chemotherapy (cytotoxic drugs) to slow the growth rate of tumours will also affect healing rates.

diseasepatients with for example rheumatoid

arthritis tend to heal more slowly

nutrition

persons who aremalnourished do not heal as quickly as those with a healthy diet.

blood supply.

since blood is the way in which food arives at the tissues, any condition where blood supply is compromised will result in delayed healing. examples you will come across include diabetes and peripheral vascular disease. this is also why tendons and ligaments heal more slowly than muscle tissue (which has a vastly superior blood supply.) fractures of the lower tibia are notoriously susceptible to delayed or non union, owing to the bone having a poor blood supply inferiorly.

the type of tissuethe type of tissue damaged dictates the ability to heal, cells of the central nervous system do not regenerate, muscle has some regenerative capacity as do cells of the lower motor neurone.

keloid scarring- in patients who have experienced severe burns, an overgrown, swollen scar may result. this is minimised by the use of pressure garments which tightly hug the skin whilst healing is taking place. keloid scarring may be a problem both cosmetically and in terms of function.

specific healing situations.

body cells are divided into three groups according to their ability to repair and regenerate.

| | | | | | labile cells stable cells permanent cells

1 labile cells.

these continue to proliferate and regenerate throughoutlife examples include skin epithelial cells, blood cells and bone cells.

2 stable cells.

these have a low normal level of regeneration, and are capable of undergoing rapid division to reconstitue the organ concerned. these constitue all the parenchymal cells of the body e.g. liver, pancreas. so if a person drinks heavily, then ceases, there is hope for his / her liver! for the normal structure of the organ to occur however, the supporting connective tissue structure must be intact, e.g. liver lobule, otherwise scarring will result.

3 permanent cells.

these are the specialised cells such as nerve and cardiac muscle cells(skeletal muscle does have some regenerative ability) these cells do not divide, once they are gone, they stay gone! The lower motor neurone will regenerate providing the cell body is intact.

the cells and tissues involved in the inflammatory response.

1 mast cell………………..connective tissue cell2 fibroblast………………connective tissue cell3 macrophage ……………connective tissue cell 4 polymorphonuclear lymphocyte …intravascular cell5 lymphocyte……………...intravascular cell6 platelets………………….intravascular cell7 monocyte……………….intravascular cell8 eosinophil……………… intravascular cell9 basophyl………………...intravascular cell10 elastin………………....connective tissue matrix11 collagen………………. connective tissue matrix12 proteoglycans………. ...connective tissue matrix

write three lines on the function of:

mast cells………………………………………………………………………………………………………………………………………….…………………………………………………………………………….fibroblasts……………………………………………………………………………………………………………………………………….……………………………………………………………………………….macrophages………………………………………………………………………………………………………………………………………..……………………………………………………………………………..polymorphonuclear lymphocytes………………………………………………………………………………………………………………………………………..……………………………………………………………………………..lymphocytes………………………………………………………….………………………………………………………………………………………………………………………………………………………….platelets…………………………………………………………………………………………………………………………………………………………………………………………………………………………monocytes……………………………………………………………………………………………………………………………………………………………………………………………………………………….eosinophils……………………………………………………………………………………………………………………………………………………………………………………………………………………….basophils…………………………………………………………………………………………………………………………………………………………………………………………………………………………..elastin…………………………………………………………………………………………………………………………………………………………………………………………………………………………….collagen……………………………………………………………………………………………………………………………………………..……………………………………………………………………………..proteoglycans/prostaglandins……………………………………………………………………………………………………………………………………..………………………………………………………………………………………………………………………………