Injury à constriction of microcirculation à dilation of microcirculation à increased permeability of blood vessels (edema) à exudates leaves the microcirculation à increased blood viscosity à decreased blood flow through microcirculation à margination (RBCs align in the center of the blood vessels and WBCs line up along the periphery) and pavementing (WBCs line up along the walls of the blood vessel) of WBCs à WBCs leave the microcirculation and enter tissue (emigration), directed by chemotaxis à WBCs ingest foreign substances

What are the 5 classic signs of inflammation?

1. -redness (erythema)
2. -heat
3. -swelling (edema)
4. -pain
5. -loss of function

Name 3 Systemic manifestations of inflammation

-fever: pyrogens act on the hypothalamus

-leukocytosis: increase in WBC count

-lymphadenopathy: enlarged nodes

Name 6 WBCs associated with emigration and chemotaxis:

1. -neutrophils: phagocytosis; 1^st responder, primary cell involved in inflammation, PMN, “eat well and die”
2. -monocytes: phagocytosis; 2^nd cell to participate, also functions in the immune response, more prevalent in chronic inflammation
3. -lymphocytes: chronic inflammation and immune response, B and T lymphocytes
4. -plasma cells: chronic inflammation and immune response
5. -eosinophils: inflammatory and immune response; allergy and asthma
6. -mast cells: inflammatory and immune response

1.  
   1. -lymphocytes #1 WBC involved (B and T)
   2. -macrophages
   3. -natural killer cells
   4. -eosinophils
   5. -mast cells

a) plasma cells: produce antibodies (immunoglobulins) M, E, A, D, G

-IgM is largest

b) b memory cells: clones itself and remembers antigen from previous exposure

-antigen + antibody= immune complex

a) t-helper: increase function of B-lymphocytes

b) T-suppressor: turn off B lymphocytes

c)T- cytotoxic: directly attack tumors or virally infected cells

d) T-memory: remembers antigen from previous exposure

2 components of the immune response

a)humoral: production of antibodies; B lymphocytes

b)cell- mediated: lymphocytes usually working solo; usually T; some macrophage involvement

* the two components work together to create specific immunity

a) active: microorganisms cause the disease; antibodies are produced in response to the antigen

-acquired: vaccine; example: HEP B

    -natural: exposed to live pathogen à     develop disease à immunity occurs (example: chicken pox; varicella zoster)

b)passive: host does not form their own antibodies; used from another person or animal ; short lived; no memory

-acquired: injection; short term; immediate immunization (accidental exposure to needle stick Hep B à given IgG)

-naturally: prior to birth; antibodies passed through placenta; nursing

Minor: most common; red hallow with yellow center; moveable oral mucosa; less than 1 cm, go away on their own; self limiting

Major: greater than 1 cm; longer duration; longer to heal; usually in posterior part of oral cavity; scarring probably present; moveable mucosa (soft palate)

Herpetiform: normally occur in groups, very painful, last weeks to months, usually on gland baring mucosa (under tongue); can also be on non moveable mucosa;  not associated with herpes virus

1. -Behcet’s syndrome
2. -Crohns disease
3. -ulcerative colitis
4. -cyclic neutropenia
5. -sprue (gluten intolerance)
6. -intestinal lymphoma
7. -HIV

1. -skin lesions: bulls eye or target form lesion
2. bleeding, cracked lips
3. acute and self limiting
4. can affect skin and oral mucosa, can have one without the other
5. can see macules to bullae
6. Stevens-Johnson syndrome is the most severe
7. refer to MD

a)reticular: most common, assoc. with Wickham Straie

b)hypertrophic: plaque like lesion; poss. Wickham Straie

c)erosive: epithelium separates from connective tissue; associated with desquamative gingivitis; red, super inflamed, looks like it is peeling off

-benign condition that can affect the skin and oral mucosa

-Wickham Straie: a pattern of interconnecting white lines and circles

-most often on the buccal mucosa

-diagnosis: made of clinical appearance

-3 types:

-abnormal immune response to a microbial antigen

-arthritis, urethritis, conjunctivitis= triad

-can see lesions on the skin and oral mucosa

-NSAIDs or aspirin used for treatment

a)Letterer-Siwe: younger than 3 yrs. of age; no oral involvement; child usually passes away before oral involvement

b)Hand-Schuller-Christian: younger than 5 yrs. old; radiolucent areas of bone-including alveolar (“punched out”); sore mouth with ulcers; loose or sore teeth; early exfoliation; chronic

c)Eosinophilic granuloma of bone: older children and young adults; skull and mandible involved; can be seen on RADS as PA abscess or periodontal disease

1. skin lesions: butterfly rash
2. lesions worsen when exposed to sun
3. can be fatal because it affects organs
4. unknown etiology, wide range of symptoms, more common in African Americans, periods of remission and exacerbation
5. oral lesions can mimic lichen planus but less symmetrical

1. -severe, progressive à potentially life threatening
2. -oral lesions: first sign in 50% of people
3. -virtually all untreated individuals show oral lesions
4. -bulla à shallow ulcer covered by grey pseudo membrane
5. -painful, erythematous below the membrane
6. -persistant if not treated
7. -Nikolsky’s sign: blow air or wipe with gauze à membrane sloughs off (Very fragile)
8. -Tzank cells present microscopically: due to loss of attachment between epi.cells
9. -acantholysis: separation of epi. cells resulting in blister formation
10. -diagnosis: microscopic and immunofluorescence
11. -treatment: team approach, corticosteroids and immunosuppressive agents, alcohol and abrasives should be avoided, gentle debridement and minimize tissue manipulation

1. mucous membrane pemphigoid,
2. benign mucous membrane pemphigoid

1. -affects: mucosa, conjunctiva, genital mucosa, skin
2. -lesions heal with scarring
3. -affects other mucous membranes besides oral
4. -autoimmune disease, chronic, may be induced by medications
5. -antibodies target the basement membrane (separation of basement membrane from the connective tissue)
6. -bulla à raw erythematous or ulcerated surface
7. -also see a positive Nikolskys sign
8. -most common site is free or attached gingival
9. -diagnosis: biopsy and histologically
10. -treatment: topical or systemic corticosteroids

1. -oral lesions not as prevalent
2. -bulla formation; same division as cicatrical
3. -no association with scarring
4. -usually affects skin first; lack of oral lesions
5. -same treatment as cicatrical

1. -caused by spirochete and fusiform
2. -painful condition with necrosis of interdental papillae
3. -grey psuedomembrane; looks like tissue sloughing
4. -punched out papilla
5. -potent smell

1. -inflammation around an impacted or partially erupted tooth
2. -bacterial in origin
3. -diagnosis: clinical
4. -treatment: lavage, antibiotics
5. -differentiate from operculum: operculum is not a bacterial infection
6. -operculum: a small flap of tissue covering the molars; usually impacted 3rds

-most common oral fungal infection, candida albicans, condition caused by overgrowth, affects superficial layer of epi.

-usually occurs in patients that are immunocomprimised

-chronic lesions in the oral cavity as well as genitally

-all need to be treated with topical or systemic anti fungal meds.:

            -Clotrimazole (Mycelex) oral troches

            -Nystatin (Mycostatin) oral suspension, ointment

            -systemic antifungals for IO: ketoconazole (Nizoral) and Fluconazole (Diflucan)

-consider underlying systemic disease if lesions return within 2-4 weeks post treatment

-avoid Listerine

-“thrush”

-mucosa is erythematous with white, curd like overlay

-wipes off à an erythematous mucosal surface

-most common on dorsal tongue, palate, denture bearing mucosa

-pt. may report burning mouth

-will not wipe off!

1. -most common type
2. -“denture stomatitis”
3. -varies from petechiae like to generalized and granular
4. -usually asymptomatic
5. -ask pt. if they take their denture out at night

1. -“candida leukoplakia”
2. -hyperplastic epithelium
3. -excess surface keratin
4. -painless
5. -persistant
6. -does not wipe off!
7. -may show signs of epithelial dysplasia à precancerous cells
8. -will respond to antifungal, if not it might be leukoplakia

1. fissures or cracks in the corners of commisures
2. -B3 niacin deficiency

1. -chronic lip sucking
2. -erythematous, cracking
3. -needs to be treated for yeast infection

1. more of a descriptive term, in order to have a wart à have to have virus present
2. -differentiate between HPV with biopsy

1. Verruca vulgaris (common wart): 
2.  Condyloma acuminatum:
3. Focal Epithelial hyperplasia:

1. direct contact
2. -can be transmitted from skin to oral mucosa
3. -white, papillary, exophytic lesion
4. -diagnosis: clinical presentation, biopsy
5. -treatment: surgical excision but may recur

1. -benign
2. -transmitted to oral cavity via oral-genital contact
3. -associated with anogenital infection
4. -red flag of sexual abuse in children
5. -types 6, 11: genital warts
6. -types 16, 18: cervical

1. -“Hecks Disease”
2. -HPV 13: multiple white-pink nodules, clusters
3. -asymptomatic
4. -resolve in a few weeks à will still have virus
5. -diagnosis: clinical presentation, biopsy 

1. -2 types: oral (HHV 1) and genital (HHV 2)
2. -primary or initial infection: primary herpetic gingivostomatitis; acute
3. -second: recurrent herpes simplex infection
4. -transmitted by direct contact
5. -virus is isolated from both primary and secondary à can hide in nerve ganglion then pop back up
6. -treatment: antiviral drugs, no cure, reduces duration; restrict contact; avoid topical xylocaine, hydrate, antipyretics, postpone dental treatment

1. 1^st outbreak of herpes
2. -painful, erythematous, swollen gingival, vesicles which progress to ulcers, fever, malaise, lymphadenopathy, firey red gingival
3. -lesions usually heal in 1-2 weeks
4. -mostly kids
5. -PHG à virus lays dormant in nerve ganglion (trigeminal) à recurrent herpes

1. -stimuli trigger viral infection
2. -prodromal signs: tingling, burning, itching
3. -differentiate from apthous ulcers: prodrum present; associated with bound down tissue (over bone)
4. -treatment: time, antiviral meds.

chicken pox

-contagious: spread by respiratory aerosols and contact with lesions

-exanthem: wide spread rash, don’t scratch

-oral lesions are not severe

-about 2 week duration

Shingles (herpes zoster)

-2^nd outbreak

-track sensory nerve

-unilateral, painful vesicle eruption

-trigger: stress, immunosuppressed, old age, malignancy or tumor growth, alcohol abuse, dental work

-prodrome: burning, itching, pain, fever, malaise, lymphadenopathy, painful

-chronic phase: postherpetic neuralgia: clinical appearance is fine but still in pain

-acute phase: IO may see white opaque vesicles to ulcers most commonly found on the buccal mucosa and attached tissue; may have ocular involvement; unilateral

a) infectious mononucleosis: “mono”

-sore throat, fever, fatigue, palatal petechiae

-diagnosis: blood test

-transmission: close contact, “kissing disease”

-treatment: treat symptoms, usually resolves in 4-6 weeks

b)hairy leukoplakia:

-lateral border of tongue (bilateral)

-immunocomprimised (HIV)

-can resemble keratinized tissue from chronic tongue chewing

-transmission: fecal-oral, saliva, respiratory droplet

-all are generally mild and short duration requiring no treatment

-diagnosis: viral culture, clinical presentation

1) Herpangina:

2) Hand Foot Mouth Disease:

3) Acute Lymphonodular Pharyngitis: