KEY TERMS

INFLAMMATION & TISSUE RESPONSE

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: A l k L h leukocyte with many forms, involved ih f i l d with chronic inflammation and immunity Mast cell: produces histamine, a vasodilator plasma cell: a specialized lymphocyte that makes antibodies

KEY TERMS
Chemotaxis: directed movement of WBCs to injury site Chemotactic factors: chemicals that cause chemotaxis Bradykinin: Kinin system chemical that causes vessel dilation pain dilation, Prostaglandins: chemical mediator causing pain, dilation, bone resorption, fever Histamine: Chemical produced by mast cells that cause dilation Serotonin: platelet chemical that constricts

KEY TERMS
Endotoxin:

cell byproducts that cause tissue damage Complement system: series of plasma proteins that regulate inflammation Microcirculation: microscopic blood vessels (capillaries, arterioles, venules) Hyperemia: increased blood flow Exudate: increased fluid at injury site Erythema: redness caused by increased blood flow

KEY TERMS
Margination:

movement of WBCs to edges of blood vessels Pavementing: attachment of WBCs to blood vessels Emigration: movement of WBCs and fluids out of blood vessels Phagocytosis: ingestion of foreign material by WBCs Pyrogens: fever producing substances Leukocytosis: increased WBC production Lymphadenopathy: enlargement of lymph nodes as WBCs mature

KEY TERMS
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

KEY POINTS
Suffix

itis defines inflammation Inflammation occurs as the initial response to tissue injury (bullet, endotoxin, etc) The process of inflammation is the same regardless of the tissue involved (gingivitis, appendicitis, appendicitis etc) The cardinal signs of inflammation are heat, redness, swelling, pain, loss of function The systemic signs of inflammation are fever, leukocytosis, lymphadenopathy

STEP 1 - INJURY

bacteria

endotoxin

Physical injury

Bacterial injury

STEP 2 VASOCONSTRICTION

STEP 3 VASODILATION 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.
Mast cell Histamine Blood Bl d vessel l

Blood vessel Serotonin released by platelets

ERYTHEMA SWELLING
Injured tissue Scrape the back of your hand to see serotonin form

HEAT
Bradykinin Prostaglandin

STEP 3 ACTIVE HYPEREMIA

STEP 3 PASSIVE HYPEREMIA

Blood vessel

Blood vessel

Normal blood amount enters but less leaves More blood enters but normal amount leaves
REPEAT

Question: Which is more problematic, active or passive hyperemia and why?

STEP 4 CHEMOTAXIS
Neutrophils (PMNs) called to area by chemotactic factors. Monocytes follow to clean the area. They are the buzzards of ACUTE inflammation. Blood vessel

STEP 5 PERMEABILITY
Dilation causes vessel wall to open allowing cells and fluids to leave. Blood vessel

monocyte

PMN

PMN

PMN

PMN

monocyte

PMN

PMN

PMN

PMN

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 PMN PMN

monocyte monocyte monocyte PMN PMN PMN PMN PMN PMN PMN PMN

PMN

PMN

monocyte

PMN

PMN

PMN

PMN

STEP 8 EXUDATION
Monocyte becomes a macrophage in interstitial tissue and ingests foreign matter macrophage monocyte PMN PMN PMN PMN

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.

lysosome lysosome lysosome

PMN Foreign matter 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. monocyte t PMN N PMN N PMN PMN

STEP 9 CHRONIC INFLAMMATION

HYPERPLASIA In response to inflammation, cells often increase in number DO NOT CONFUSE WITH

lymphocyte

Plasma cell

ANTIBODIES

lymphocyte

Plasma cell

HYPERTROPHY In response to stimulation, cells increase in size

STEP 10 - HEALING
Day of injury clot forms, consists of fibrin, RBCs and platelets One day after injury - acute inflammation Two days after injury

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)

Monocytes become macrophages Granulation tissue forms (fibroblasts and capillaries) Lymphocytes, plasma cells emigrate

10 MINUTE
BREAK
REST YOUR INFLAMMED BRAINS

INJURIES TO ORAL TISSUES

Tooth

related inflammatory responses Soft tissue trauma Nicotine stomatitis Salivary gland conditions Granulomas Irritation fibroma Hyperplasia

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

AMALGAM TATTOO
Caused

resorbed abnormally Resorption normal during exfoliation Orthodontics can cause it

by amalgam scraps in tissue A macule Usually giant cells present (several macrophages joined together), engulf scraps Harmless

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 exam fibroblasts, lymphocytes, plasma cells, macrophages Often must be removed before healing can occur
Microscopic

ACUTE ABSCESS
Extremely Pulp

PERIAPICAL (RADICULAR)
CYST

painful tissue necrosing, producing exudate, gas Microscopic exam reveals neutrophils, macrophages

Inflammatory

bi-products stimulate stray epithelial ti l t t ith li l cells to grow form an epithelial lined sac Often asymptomatic

ALVEOLAR OSTEITIS
dry socket Post operative complication after extraction, usually mandibular 3rd molar Caused by early loss of y y clot Severe pain, bad taste, odor Treat symptoms, warm rinses, medicated packing

HYPERPLASTIC PULPITIS
Seen

in children with large, open lesions Granulation tissue containing chronic inflammatory cells

OSTEOMYELITIS
CONDENSING OSTEITIS
Bone

becomes infected after tooth removal May start as dry socket Necrotic bone must be removed, resutured

When

periapical lesion heals, bone is replaced Bone is disorganized, contains no trabeculae Appears radiopaque

ASPIRIN BURN
Patient

TRAUMA
Oral

places aspirin on tooth to relieve toothache, Hyperkeratosis from acid attack,

lesions have a variety of etiologies, tongue biting after anesthesia, burns, h i b cheek biting (linea alba) Warn children not to chew tongue after mandibular block

FIBROMA
Most

MUCOCELE
Also

common oral lesion Excessive fibrous f tissue after healing Contains fibroblasts, sessile, pink in usually a health pink color

called mucous retention phenomenon S li Saliva leaks into l k i connective tissue from damaged minor salivary gland Often seen on lower lip, reoccurs

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SOLAR CHEILITIS MELANOSIS

Melanocytes Leathery, Most

activated to produce melanin for unknown reasons Women affected more than men. Associated with trauma, smoking

corrugated lip or skin often the lower lip May become cancerous

NICOTINE STOMATITIS
Characteristic

PAPILLARY HYPERPLASIA
Also

clinical appearance red dot (inflamed salivary duct) surrounded by white, keratinized tissue i

called palatal papillomatosis Pebbly appearance Clinically diagnostic g Usually requires removal before new denture

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EPULIS FISSURATUM

DENTURE STOMATITIS
Inflammatory

Hyperplastic

oral mucosa caused by ill fitting denture E i Excise tissue, i remake denture

response to denture material May require new denture from another material Instruct patient to leave denture out more often

RANULA
Whartons

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

duct blocked by sialolith (salivary stone) causes unilateral swelling in floor of mouth th May lead to acute or chronic sialadenitis (inflammation of a salivary gland)

What duct is this?

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PYOGENIC GRANULOMA
Exuberant healing with excessive granulation tissue Sometimes called pregnancy tumor but common in males Contains fibroplasts, capillaries, capillaries inflammatory cells but none are pus producing

CENTRAL GIANT CELL GRANULOMA

Central is in bone, peripheral is in soft tissue Both contain giant cells, chronic inflammation 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

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