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Perio - Exam 2 > Exam II - Lecture I > Flashcards

Exam II - Lecture I Flashcards

1
Q

What are the 5 cardinal signs of inflammation?

A

Redness - rubor

Swelling - tumor

Heat - calor

Pain - dolor

Loss of function - Functio laesa

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2
Q

What is the most important thing in innate immunity?

A

Intact tissue

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3
Q

Innate immunity consists of what?

A

Serum complement

Neutrophil

Monocyte-macrophage

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4
Q

What is the line b/t acute inflammation and chronic inflammation?

A

When monocytes-macrophages get involved, then it goes to chronic and usually involves acquired immunity

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5
Q

Acquired immunity has what cells?

A

Lymphocytes

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6
Q

What leads to a systemic infection?

A

Lymphocytes cannot handle the infection

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7
Q

Probing depth is a _________ finding.

Pocket depth is a _________ finding.

A

Clinical

Histological

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8
Q

Tell me some factors of the histopathology of periodontal disease.

A

Increased epithelial turnover rate

Increased # of blood vessels

Destruction of collagen fiber network

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9
Q

Tell me histologic symptoms of an initial lesion of periodontitis. 6 symptoms.

A

1- Classic vasculitits of vessels subjacent to the JE

2- Exudate

3- Increased migration of leukocytes into the JE and sulcus

4- Presence of serum proteins, esp fibrin

5- Alteration of the most coronal portion of the JE

6- Loss of perivascular collagen

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10
Q

Tell me clinical symptoms of an initial lesion of periodontitis.

A

Appears clinically healthy

No pocketing

No radiographic evidence of bone loss

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11
Q

Tell me 5 histologic symptoms of an early lesion of periodontitis.

A

1- Accentuation of features of the initial lesion

2- Accumulation of lymphoid cells subjacent to JE

3- Cytopathic alterations of fibroblasts

4- Further loss of collagen fiber network of the marginal gingiva

5- Beginning proliferation of basal cells of JE

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12
Q

Tell me 4 clinical symptoms of an early lesion of periodontitis.

A

1- Gingivitis (acute)

2- Changes In gingival color, contour, consistency, and BOP

3- No pocketing

4- No bone loss

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13
Q

Tell me 6 histologic symptoms of an established lesion of periodontitis.

A
  • Persistence of the symptoms of the acute inflammation
  • Predominance of plasma cells w/o appreciable bone loss
  • Presence of immunoglobulins extravascularly in the CT an dJE
  • Continuing loss of CT noted in early lesion
  • Proliferation, apical migration, and lateral extension of JE
  • Early pocket formation +/-
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14
Q

Tell me 4 clinical symptoms of an established lesion of periodontitis.

A
  • Gingivitis (Chronic form)
  • Changes in gingival color, contour, consistency, and BOP
  • No pocketing
  • No bone loss
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15
Q

Tell me 8 histologic symptoms of an advanced lesion of periodontitis.

A
  • All features of established lesion
  • Extension into alveolar bone and PDL w/ significant bone loss
  • Continuous loss of collagen
  • Altered plasma cells
  • Formation of pockets
  • Periods of quiescence and exacerbation
  • Conversion of distant bone marrow into fibrous CT
  • Widespread manifestations of inflammation
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16
Q

Tell me 4 clinical symptoms of an advanced lesion of periodontitis.

A
  • Periodontitis
  • Changes in gingival color, contour, consistency, and BOP
  • Periodontal pocket formation
  • Alveolar bone loss as shown on radiographs
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17
Q

Periodontitis in children is evidenced by the presence of ___________, not plasma cells.

A

Lymphocytes

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18
Q

Periodontitis in adults is characterized by presence of _________.

A

Plasma cells

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19
Q

FAs, FMLP, and LPS attract what?

A

PMNs

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20
Q

What is the current model of periodontitis?

A

Microbial challenge ->Host Immune-inflammatory response -> CT and bone metabolism -> Clinical signs of disease initiation and progression

*Genetic risk, environmental, and acquired risk factors lead into this as well

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21
Q

Those that get aggressive periodontitis are said to be _____-________.

A

HYPER-Responsive

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22
Q

Those that are said to have no response to a bacterial challenge are called _____-________.

A

HYPO-Responsive

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23
Q

Tell me the critical pathway model of pathogenesis.

A

Pathogenic flora->immune response (Complement, mast cells, antibodies, neutrophil clearance)

IF clearance does not occur, then what?
-Bacterial penetration
—Either a systemic exposure, or
—Monocyte, lymphocyte axis
—-Initial periodontitis has begun
-Leads to cytokines, inflammation and tissue destruction, pocketing and bone loss
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24
Q

What attacks plaque?

A

Mast cells

Acute phase proteins

Complement

PMNs

Antibodies (Adaptive)

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25
Q

What do mast cells have in them?

A

Granules

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26
Q

Mast cells release ________ which cause vasodilation.

A

Histamine

*Also Fc fragments and IgE

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27
Q

T/F - Mast cells have granules.

A

TRUE

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28
Q

The etiology of gingivitis, periodontitis, and caries is what?

A

PLAQUE BIOFILM

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29
Q

T/F - Gingivitis is due to the host response.

A

TRUE

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30
Q

T/F - >90% of Americans have periodontal disease (Gingivitis). ~50% of Americans have periodontitis.

A

TRUE

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31
Q

What WBC is one of the 1st responders to an infection?

A

MAST Cell

  • Granules
  • No phagocytosis
  • Comes from myeloid stem cell line
  • -Common receptor is the Fc fragment receptor of IgE*
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32
Q

What activates and causes anaphylaxis?

A

MAST CELLS

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33
Q

What do mast cells release? 6 things

A

Histamine (Vasoactive amines)

Eosinophil chemotactic factor

Platelet activating factor

Enzymes

Leukotrienes C, D, E

Prostaglandin PGD2, thromboxane

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34
Q

T/F - Anaphylaxis can happen from latex and/or rubber gloves.

A

TRUE

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35
Q

T/F - According to Winkler, C3a binds on the surface of the mast cell.

A

TRUE

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36
Q

What is histamine SRSA?

A

Slow reacting substance A

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37
Q

What releases interleukins?

A

ONLY WBCs

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38
Q

Vasodilation does what to blood flow?

A

SLOWS IT DOWN

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39
Q

In order to get WBCs to the site, what must happen?

A

Vasodilation of vessel to slow blood flow

Permeability of vessel must increase to get the WBCs thru the endothelium

40
Q

What happens in response to tissue injury?

A

Release of chemical mediators that increase permeability of adj small blood vessels

41
Q

What happens when blood vessels are dilated and increased permeability to plasma?

A

Tissues swell due to plasma leakage

Elevated temp from increased blood flow

Redness

Pain from increased fluid in tissues and direct effect of chemicals on sensory nerve endings

42
Q

What happens when circulating WBC adhere to walls of altered blood vessels?

A

WBC chemotaxis thru vessel walls and to area of injury

This induces phagocytosis of foreign material and tissue debris and initiation of Ab production

43
Q

Make a card at 57 minutes (Slide 27)

A

CARD

44
Q

Histamine has what effects?

A

Dilation of increase of permeability of small blood vessels : constriction of bronchi

45
Q

Chemotactic factors have what effects?

A

Eosinophil and PMN chemotaxis

46
Q

T/F - Interleukins 3,4,5,6 have many effects.

A

TRUE

47
Q

Mast cells release what chemicals that cause effects? 6 things

A

Histamine

Chemotactic factors

Interleukins 3,4,5,6

TNF-alpha

Leukotrienes

Prostaglandins

48
Q

TNF-alpha has what effects?

A

Recruitment of granulocytes to area of inflammation - inducement of fever

49
Q

Leukotrienes have what effects?

A

Dilation of small blood vessels

Constriction of bronchi

Chemotaxis of leukocytes

50
Q

Prostaglandins have what effects?

A

Increase in vascular permeability

Regulation of immune responses

51
Q

What are acute phase proteins?

A

Proteins whose plasma concentrations increase or decreases

Increase - Positive acute-phase proteins

Decrease - Negative acute-phase proteins - this is in response to inflammation

52
Q

What plasma proteins are increased due to microbial infection? 6 of them.

A

C-reactive protein

Fibrinogen

Complement

Mannose-binding protein

Metal-binding proteins

(These 5 are associated with increased risk of heart disease)

Alpha1-antitrypsin, alpha1-anticymotrypsin

53
Q

What are 2 well established risk factors for cardiovascular disease?

A

Tobacco smoking

High LDL

54
Q

Recent evidence has identified __________ __________ as an important risk factor for MI, like a 2-5 fold increased risk

A

C-reactive protein

**This is a better indicator of risk over tobacco smoking or high LDL

55
Q

Where is complement synthesized? (In what organs?)

A

Liver
-Risk of bone infection if a liver problem is also present

Small intestine

Macrophages

Other mononuclear cells

56
Q

Understand complement

A

Seriously.

57
Q

T/F - PMNs have granules.

A

TRUE

58
Q

A non stimulated PMN is what?

A

Round

59
Q

A stimulated PMN is what shape?

A

Takes a bipolar shape

-It’s a shapeshifter

60
Q

T/F - PMN comes from a myeloid stem cell.

A

TRUE

61
Q

What does never let mean eat burritos mean?

A

Most common WBCs in the blood

Neutrophils

Lymphocytes

Macrophages

Eosinophils

Basophils

62
Q

Tell me about neutrophils.

A

Lobed nucleus

Granules

Most of the circulating leukocytes

Phagocytosis of bacteria

63
Q

If an infection is present, what happens to PMNs?

A

Large increase in PMNs

64
Q

Tell me about eosinophils?

A

Granules

Few in tissues

Inflammatory

65
Q

Tell me about basophils.

A

Lobed nucleus

Granules

Tissues

Release histamine

66
Q

Tell me about monocytes.

  • Macrophages
  • Dendritic cells
A

Single nucleus

All tissues and linings

Phagocytosis and presenting of cells

67
Q

What is the half life of a PMN?

A
  • 5 to 90 days*

- Die in spleen or killed by infection

68
Q

Name three things PMNs do.

A

Phagocytosis

Release of enzymes

Release of chemical mediators

69
Q

Tell me the movement of PMNs.

A

Leaves circulation to get to site of action by squeezing through endothelium

  • Sticks to endothelium (selectins, adhesins)
  • Squeeze thru endothelium (diapedesis)
  • Chemotaxis (inflammatory mediators)
  • Phagocytosis
  • Death (apoptosis)
70
Q

What is in the phagolysosome?

A

Proteolytic enzymes

When these phagocytosize things, they degrade and cause local tissue damage

71
Q

Cellular adherence molecules (ICAM-1,2 and ELAM) do what?

A

Tell PMNs to stop at that site

72
Q

IL-8 does what?

A

Modifies the endothelium

73
Q

Tell me the difference b/t chemokinesis and chemotaxis.

A

Chemokinesis - Live cells will move when stimulated
-*Except for KERATINOCYTES
—They are full of keratin and dead

Chemotaxis - Directed movement of WBCs toward a chemotactic gradient

74
Q

What granules are in PMNs?

A

Primary - (azurophilic)

Secondary - (specific)

Tertiary

75
Q

What are the 5 general steps of phagocytosis?

A

Bacterium is bound

Brought into phagosome

Phagosome and lysosome combine for the phagolysosome

Bacteria degraded

Bacterial debris is exocytosed

76
Q

What two important receptors are on the surface of PMNs?

A

Fc fragment receptor

C3b receptor

77
Q

Primary/azurophilic granules. Tell me.

A

Myeloperoxidase

Bactericidal/permeability-increasing protein (BPI)

Defensins

Elastase - SERINE PROTEASE

Cathepsin G - SERINE PROTEASE

78
Q

Specific granules (secondary granules). Tell me.

A

Alkaline phosphatase

Lysozyme

NADPH oxidase

Collagenase

Lactoferrin

Cathelicidin

79
Q

Tertiary granules. Tell me.

A

Cathepsin

Gelatinase

80
Q

What are some oxygen dependent microbiocidal mechanisms?

A

NADPH oxidase complex

Myeloperoxidase

Superoxide dismutase

81
Q

What are some O2 independent microbicidal mechanisms?

A

Serine Proteases

Acid hydrolases

Metalloproteinases

Lysozyme

Bactericidalensins

82
Q

T/F - Fibroblasts release a lot of collagenase which causes self-tissue damage by cutting tissue into 1/3 and 2/3 fragments.

A

TRUE

83
Q

Tell me about elastase.

A

SERINE PROTEASE

Highly active non-specific protease

84
Q

Collagenase/Gelatinase does what?

A

Breakdown collagen

  • Released as proenzyme
  • Gets to environment and is cleaved into the active enzyme
85
Q

What are 3 reasons that neutrophil proteases are NOT thought to be significantly involved in tissue damage?

A

Tissue bathed in plasma anti-proteases

Metalloproteases are released in a latent inactive form

Anti-oxidants exert strong anti-inflammatory effects in neutrophil-dependent tissue damage model systems

*TIMPs - Tissue inhibitors metalloproteases

86
Q

What can HOCL do?

A

Oxidatively inactivate 3 major tissue anti-proteases

Can oxidatively activate collagenase and gelatinase - these are released as proenzymes

87
Q

T/F - Nonoxidative PMN enzymes bind metal.

A

TRUE

*Most common way to deal with stuff

88
Q

What is a PMN respiratory burst?

A

PMNs can glow
-Chemoluminescent

Reactive species from bleach and H2O2

89
Q

T/F - There is a quantitative and qualitative aspect to PMN immunology.

A

TRUE

Must be sufficient number of them, and must be properly functioning in immunity

90
Q

What 5 things are associated with PMN immunology?

A

Quantitative/Qualitative

Chemotaxis/Chemokinesis

Phagocytosis

Killing

Respiratory burst

91
Q

What are 4 host risk factors associated with modifiers of disease expression genetic/induced neutrophil defects - decreased killing, dysregulation?

A

Leukocyte adhesion deficiency (LAD)

Papillon LeFevre Syndrome

Diabetes

Smoking

92
Q

What are 2 types of healthy gingiva?

A

Pristine
-Little to no inflammatory infiltrate

Clinically healthy state
-Inflitrate is present, but this is normal

93
Q

T/F - The apical termination of the JE is at the CEJ in gingivitis.

A

TRUE

94
Q

What happens in gingivitis?

A

Sulcus has deepened and changed into pocket epithelium

Gingival CT near the PE is heavily infiltrated with inflammatory cells
-PMNs, T-lymphocytes, few plasma cells

PE into inflamed CT

No apical migration of the JE or resorption of alveolar bone has occurred

95
Q

Histologically, gingivitis. Talk about it.

A

PMNs

T lymphocytes w/ lesser number of plasma cells

96
Q

Histologically, periodontitis. Tell me.

A

JE has converted to an ulcerate PE that is located on the root surface apical to the crest of the alveolar bone

ICGT underlying the PE has been replace with a heavy inflammation

Perio - Exam 2 (8 decks)

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