Inflammatory Process/Acute Inflammation/Chronic Inflammation Flashcards
main goal of inflammatory process
to repair tissue, destruction of healthy tissue occurs in the process
exogenous element
physical, chemical and mechanical injuries
pathogenic organisms
endogenous elements
genetic
immune dysfunction or deficiency
degenerative
two major kinds of inflammation
acute: limited in area and duration, cardinal signs
chronic: long duration or history of repeated insults or injuries
what suffix is for inflammation of an area
‘itis’
three phases of acute inflammation
- Initiation (Events 1-5)
- Amplification (Events 6 & 7)
- Termination (Event 8)
initiation
activated when injury occurs
changes to microcirculation
loss of fluid from blood into tissues
white blood cells move to area
amplification
chemical mediators direct more and different types of white blood cells into the injured area
increasing response and neutralizing agents causing the response
termination
requires other chemical substances to stop or inhibit inflammatory process
if it continues, more damage will result
event 1
vasoconstriction of microcirculation controls bleeding
-chemical mediators released
-lasts a few minutes only
event 2
vasodilation
-more blood flows into the area
-chemical mediators are released
event 3
blood vessel become permeable
-fluid or exudate leaves vessels
-chemical mediators
-signs of inflammation evident
cardinal signs of inflammation
- heat
- redness, hyperemia
- swelling
- pain
- loss of function
event 4
vascular stasis (slowing of blood)
-margination (WBCs move to vessel’s walls)
-pavementing (WBCs adhere to walls)
-transmigration (WBCs squeeze through vessel walls)
-plasma fluid is lost, blood vessels thicker
-red blood cells to center of vessels
event 5
chemotaxis
-cells directed by chemical mediators to move in a specified direction
-WBCs ‘attracted to’ or ‘driven to’ injury
event 6
opsonization (cell death)
-opsonins (immunoglobin) found in exudate
-organisms coated with opsonins
-leukocytes prepare foreign organisms for phagocytosis
event 7
phagocytosis
-foreign matter eliminated or destroyed by phagocytosis
-if injury is extensive, more chemical mediators
event 8
termination of process
-foreign material and debris removed through lymphatic system
-chemical mediators will inhibit or stop further action by inflammatory process and area will complete healing or repair process
what do systemic manifestations do and examples
help control the injury
encourage removal of offending agents and debris association with the IP
start repair process
depends on the extent and length of the IP
does not always occur
pyrexia, leukocytosis, lymphadenopathy
pyrexia
fever
destroys pathogens by creating a higher temp and mobilize WBC
can be caused by non-infectious agents as well, dehydration and excess thyroid hormone
leukocytosis
increase of WBC
neutrophils: respond to bacteria, inflammatory disorders and certain drugs
lymphocytes: respond to viruses
monocytes: predominate in chronic infections
lymphadenopathy
swollen lymph nodes
outcomes of acute inflammation
no tissue damage: may progress to chronic inflammation or resolves completely
tissue damage: may progress to chronic inflammation, abscess formation, resolution of the inflammatory process, regeneration, repair
chronic inflammation
longer than 2 weeks = chronic inflammation
can happen without preceding acute inflammation (Chronic Periodontitis)
large number of mononuclear cells in tissue
TISSUE DESTRUCTION
steps of chronic inflammation
- macrophages driven to area by chemotactic agents from Neutrophil and from chemical mediators
- macrophages secrete more chemokines to recruit more monocytes from blood vessels where they will become macrophages
- other chemical mediators released by macrophages stimulate or enhance lymphocyte actions
what plays a role in tissue destruction while performing their job
macrophages
what causes bone and tissue destruction during chronic periodontitis
lysosomal enzymes that leak out of cells into surrounding tissues can destroy normal cells and collagen fibers in the area and can activate osteoclasts causing bone destruction
granulomatous inflammation
a subset of chronic inflammation that form granulomas
contain giant cells (macrophages) and other inflammatory cells
surround a type of foreign matter
forms a wall around the substance to prevent spread
abscess formation
when pyogenic or pus-forming microbes and enzymes enter the tissue
attracts leukocytes
if resistant to phagocytosis the tissues in the area are destroyed due to the death of neutrophils and resulting lysosomal enzyme release
resulting debris accumulates as exudate forming an abscess
fistula
when enzymes that are released by macrophages bore through the tissues following the path of least resistance allowing the exudate to flow into another area or to find a path to the outside
how do teeth become abscessed
death of the pulp and associated tissues
-cellulitis
-ludwigs angina
-bacteremia
-septicemia
-cavernous sinus thrombosis
resolution of inflammatory process
if not caused by trauma it goes away
if tissue damage healing can only begin when etiology is removed it can result in regeneration or scarring
regeneration and tissues that can and cannot
the body’s attempt to restore itself
epithelium and liver can regenerate
cardiac and nerve cannot
fibrous repair
recreates a near-normal architecture but not normal function
types of fibrous repair
primary intention: wound margins are clean and held together, migrating epithelial cells have little distance to travel
secondary intention: edges of wound cannot be brought together, begins at base and proceed bottom to top
process of fibrous repair
- initiated almost immediately after injury
- blood clot forms; fibroblasts and vascular endothelial cells appear
- angiogenesis: endothelial cells form new blood vessels; fibroblasts form collagen fibers
- formation of granulation tissue: forms framework, becomes less vascular
- epithelialization: epithelial cells grow across lower edges of wound forming basement membrane and normal stratified squamous epithelium
factors affecting wound healing
type, size, location, vascularity, infection, foreign material, excessive granulation tissue, systemic factors
complications of wound healing
inadequate scar formation: inadequate amount of granulation tissue
excessive scar formation: keloid
wound contracture: can cause mobility limitations
tooth extraction: bone and soft tissue repair
- extraction
- blood clot formation
- angiogenesis: 10 to 12 days
- bone formation: osteoblasts
- alveolar process remodeled
- replaced with spongy bone: filled in 12 weeks
dry socket
initial blood clot is disrupted and bone surface becomes exposed and necrotic
2-4 days after extraction
alveolar osteitis
alveolar osteitis
necrotic bone must be resorbed by the body and granulation tissue must form along the walls of the socket instead of within a clot
