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8/2/2019 Inflammation and Response in Various Tissues SHOW 1st [Compatibility Mode]
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INFLAMMATION
TISSUE RESPONSE
KEYTERMS
White blood cell: abbreviated WBC, a leukocyte
Stem cell: precursor for all leukocytes
Neutrophil: A polymorphonuclear leukocyte (PMN),60% of all WBCs
Monocyte: A leukocyte that becomes a macrophage
Lymphocyte: eu ocyte w t many orms, nvo vewith chronic inflammation and immunity
Mast cell: produces histamine, a vasodilator
plasma cell: a specialized lymphocyte that makesantibodies
KEYTERMS
Chemotaxis: directed movement of WBCs toinjury site
Chemotactic factors: chemicals that causechemotaxis
Bradykinin: Kinin system chemical that causes,
Prostaglandins : chemical mediator causing pain,dilation, bone resorption, fever
Histamine: Chemical produced by mast cells thatcause dilation
Serotonin: platelet chemical that constricts
KEYTERMS
Endotoxin: cell byproducts that causetissue damage
Complement system: series of plasmaproteins that regulate inflammation
vessels (capillaries, arterioles, venules)
Hyperemia: increased blood flowExudate: increased fluid at injury site
Erythema: redness caused by increased
blood flow
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KEYTERMS
Margination: movement of WBCs to edgesof blood vessels
Pavementing: attachment of WBCs to bloodvessels
Emigration: movement of WBCs and fluids
Phagocytosis: ingestion of foreign materialby WBCs
Pyrogens: fever producing substances
Leukocytosis: increased WBC production
Lymphadenopathy: enlargement of lymphnodes as WBCs mature
KEYTERMS
Hyperplasia: increased number of cells
Hypertrophy: increased size of cells
Granulation tissue: early healing tissue
composed of capillaries and fibroblasts
Keloid: excessive scar tissue
Restitution: healing without scar tissue
KEYPOINTS
Suffix itis defines inflammation
Inflammation occurs as the initial responseto tissue injury (bullet, endotoxin, etc)
The process of inflammation is the sameregardless of the tissue involved (gingivitis,
,
The cardinal signs of inflammation areheat, redness, swelling, pain, loss offunction
The systemic signs of inflammation are
fever, leukocytosis, lymphadenopathy
STEP 1 - INJURY
bacteria
Physical injury
endotoxin
Bacterial injury
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STEP 2 VASOCONSTRICTION
Blood vessel
Injured tissue
Scrape the back of your hand to see serotonin form
STEP 3 VASODILATION
Mast cell
Histamine
Vessels initially dilate when mast cells release histamine and the kinin
system releases bradykinin. A short time later, prostaglandins is
produced causing vasodilation and pain.
Blood vessel
HEAT
ERYTHEMASWELLING
Bradykinin Prostaglandin
STEP 3 ACTIVE HYPEREMIA
Blood vessel
More blood enters but normal amount leaves
STEP 3 PASSIVE HYPEREMIA
Blood vessel
Normal blood amount enters but less leaves
Question: Which is more problematic,
active or passive hyperemia and why?REPEAT
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STEP 4 CHEMOTAXIS
Blood vessel
Neutrophils (PMNs) called to area by chemotactic factors.
Monocytes follow to clean the area. They are the buzzards of
ACUTE inflammation.
PMN PMN PMN PMNmonocyte
STEP 5 PERMEABILITY
Blood vessel
Dilation causes vessel wall to open allowing
cells and fluids to leave.
PMN PMN PMN PMNmonocyte
STEP 6 MARGINATION AND PAVEMENTING
Cells move to outer margins of vessel and attach there.
PMN PMN PMN PMNmonocyte
PMN PMN PMN PMNmonocyte
STEP 7 EXUDATION
Cells and fluids exit vessel into tissue
PMN PMN PMN PMNmonocyte
PMN PMN PMN PMNmonocyte
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STEP 8 EXUDATION
Monocyte becomes a macrophage in interstitial tissue and
ingests foreign matter
PMN PMN PMN PMNmonocytemacrophage
STEP 8 EXUDATION
PMNs also ingest foreign matter and destroy it with
an enzyme (lysosome). When the PMN dies,
lysosomal enzymes are released and injure tissue.
Foreign matter
lysosome
PMN
lysosomelysosome
Purulent exudate is dead neutrophils and dead cells
STEP 9 CHRONIC INFLAMMATION
If neutrophils and macrophages cannot control inflammation,
lymphocytes and plasma cells appear. Plasma cells produce
antibodies. Inflammation is then considered CHRONIC.
PMN PMN
lymphocyte
monocyte
Plasma cell
Plasma cell
lymphocyte
ANTIBODIES
STEP 9 CHRONIC INFLAMMATION
HYPERPLASIA
In response to inflammation,
cells often increase in number
HYPERTROPHY
In response to stimulation,cells increase in size
DO NOT CONFUSE WITH
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STEP 10 - HEALING
Day of injury clot forms, consists of fibrin,
RBCs and platelets
One day after injury - acute inflammation
Two days after injury
Monocytes become macrophages
Granulation tissue forms (fibroblasts and capillaries)
Lymphocytes, plasma cells emigrate
STEP 10 HEALING (CONTINUED)
Seven days after injury fibrin is digested and
initial repair is complete, inflammation has
terminated
Two weeks after injury granulation tissue
replaced by either scar tissue (keloids) or original
tissue (restitution)
1010 MINUTEMINUTE
BREAKBREAK
REST YOURREST YOUR
INFLAMMED BRAINSINFLAMMED BRAINS
INJURIES TO ORAL TISSUES
Tooth related inflammatory responses
Soft tissue trauma
Nicotine stomatitis
Salivary gland conditions
Granulomas
Irritation fibroma
Hyperplasia
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TOOTH RELATED INJURIES
Internal and external resorption
Periapical abscess, cyst and granuloma
Hyperplastic pulpitis
Amalgam tattoo
Tooth related injuries not related to
inflammation response (attrition, abfraction,
abrasion, erosion)
INTERNAL RESORPTION
Clast cells activated
by inflammation
Root canal
necessary, not
always successful
EXTERNAL RESORPTION
Tooth resorbed
abnormally
Resorption normal
during exfoliation
Orthodontics can
cause it
AMALGAM TATTOO
Caused by amalgam
scraps in tissue
A macule
Usually giant cells
present (several
macrophages joined
together), engulf
scrapsHarmless
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PERIAPICAL LESIONS
Bone loss at apex caused by
inflammatory byproducts
exiting apex
Periapical abscess if acute
cells present (PMNs), lots of
pain
Granuloma if fibroblasts
present, a chronic condition
Cyst if it has an epithelial
lining lining
How do you know, the
difference? You dont
DENTAL GRANULOMA
Chronic response
Microscopic exam
fibroblasts,
lymphocytes,
plasma cells,
macrophages
Often must be
removed before
healing can occur
ACUTEABSCESS
Extremely painful
Pulp tissue
necrosing,
producing exudate,
gas
Microscopic exam
reveals neutrophils,
macrophages
PERIAPICAL
(RADICULAR)
CYST
Inflammatory bi-products
st mu ate stray ep t e a
cells to grow
form an epithelial lined
sac
Often asymptomatic
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ALVEOLAR OSTEITIS
dry socket
Post operativecomplication afterextraction, usuallymandibular 3rd molar
Caused by early loss ofclot
Severe pain, bad taste,odor
Treat symptoms, warmrinses, medicatedpacking
HYPERPLASTIC PULPITIS
Seen in children with
large, open lesions
Granulation tissue
containing chronic
inflammator cells
OSTEOMYELITIS
Bone becomes
infected after tooth
removal
May start as dry
socket
Necrotic bone must
be removed,
resutured
CONDENSING OSTEITIS
When periapical
lesion heals, bone is
replaced
Bone is
disorganized,
contains no
trabeculae
Appears radiopaque
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MELANOSIS
Melanocytes activated
to produce melanin for
unknown reasons
Women affected more
than men.
Associated with
trauma, smoking
SOLAR CHEILITIS
Leathery, corrugated lip or skin
Most often the lower lip
May become cancerous
NICOTINE STOMATITIS
Characteristic clinical
appearance red dot
(inflamed salivary
duct) surrounded by
white, keratinized
tissue
PAPILLARYHYPERPLASIA
Also called palatal
papillomatosis
Pebbly appearance
Clinically
diagnostic
Usually requires
removal before new
denture
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EPULIS FISSURATUM
Hyperplastic oral
mucosa caused by
ill fitting denture
xc se t ssue,
remake denture
DENTURE STOMATITIS
Inflammatory
response to denture
material
May require new
denture from
another material
Instruct patient to
leave denture out
more often
RANULAWhartons duct
blocked by sialolith
(salivary stone)
causes unilateral
swelling in floor of
mou
May lead to acute or
chronic sialadenitis
(inflammation of a
salivary gland)
What duct is this?
DRUG /HORMONE INDUCED HYPERPLASIA
Three drugs: phenytoin
(seizures), calcium channel
blockers (cardiovascular), and
cyclosporin (transplants) can
cause gingival hyperplasia in
response to inflammation
Hormonal changes due to
pregnancy, puberty can cause
hyperplasia
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PYOGENIC GRANULOMA
Exuberant healing with
excessive granulation tissue
Sometimes called pregnancy
tumor but common in males
Contains fibroplasts,
,
cells but none are pus
producing
CENTRAL GIANT CELL GRANULOMA
Central is in bone,
peripheral is in soft tissue
Both contain giant cells,
Central be a uni- or
multilocular radiolucent
mass
Roots of teeth may diverge
PERIPHERAL GIANT CELL GRANULOMA
Found in soft tissue
May resemble a
pyogenic granuloma