inflammation and response in various tissues show 1st [compatibility mode]

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.


STEP 6 MARGINATION AND PAVEMENTING

Cells move to outer margins of vessel and attach there.



STEP 7 EXUDATION

Cells and fluids exit vessel into tissue




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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

inflammation and response in various tissues show 1st [compatibility mode]

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