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Periodontics > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

How do you define periodontal health?

1) clinical gingival health on an ________ periodontium

  • BOP
  • no probing depth greater than ____mm
  • requires introduction of ____ as part of the routine dental exam to identify cases of health and gingivitis and monitor treated subjects

2) clinical gingival health on a ________ periodontium

  • ______ periodontitis patient
  • _______ periodontitis patient
A

1) intact

  • <10%
  • 3mm
  • BOP

2) reduced

  • stable
  • stable non-periodontitis
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2
Q

How do we define gingivitis? What criteria is essential for a diagnosis of gingivitis?

gingivitis _____ induced

  • associated with ____ alone
  • mediated by:
  • what are the factors?
  • drug induced gingival enlargement due to?

gingivitis ____ induced

  • what are the factors?
A

Gingivitis – dental biofilm induced

  • Associated with dental biofilm alone
  • Mediated by systemic or local risk factors
    • Sex steroid hormones
    • Hyperglycemia
    • Leukemia
    • Smoking
    • Malnutrition
    • Oral factors enhancing plaque accumulation
  • Drug-influenced gingival enlargement
    • Antiepileptic drugs
    • Calcium channel blockers
    • High dose oral contraceptives
  • Most common form of gingival disease
  • Caused by interaction of microorganisms in plaque and tissue and the inflammatory cells of the host

Gingivitis – non dental biofilm induced

  • Genetic/developmental disorders
  • Specific infections
  • Inflammatory and immune conditions
  • Reactive processes
  • Neoplasms
  • Endocrine, nutritional and metabolic diseases
  • Traumatic lesions
  • Gingival pigmentation
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3
Q

what are the symptoms and findings of necrotizing disease?

NG

NP

A

Infectious, but host immune response is critical in pathogenesis

Occur with low frequency but require immediate attention

  • NG
    • Painful
    • Necrosis and ulcer of papilla
    • Spontaneous bleeding
    • Pseudo membrane formation
    • Halitosis
    • Adenopathy or fever
  • NP (in addition to above criteria)
    • Bone destruction or sequestrum
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4
Q

what is the purpose of staging?

What is the purpose of grading?

A

staging

  • Attempt to classify severity and extent of disease
  • Assess specific factors that contribute to case
  • Important element is to explore the reason for previous tooth loss to determine loss due to periodontitis
  • Initial stage should be determined using clinical attachment loss (CAL

Grading

  • To indicate rate of progression
  • To indicate responsiveness to standard therapy
  • To indicate potential impact on systemic health
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5
Q

endemic

examples

A

habitual presence of a disease within a given geographic area

  • Usual occurrence of a given disease within such an area
  • Examples: malaria
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6
Q

epidemic

A

occurrence in a community or region of a group of illnesses of similar nature, clearly in excess of normal expectancy, and derived from a common or propagated source

  • examples: West nile virus, Ebola, SARS, Marburg virus, Avian flu
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7
Q

pandemic

A

worldwide epidemic

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8
Q

sensitivity

A

proportion of subjects with disease who test positive

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9
Q

Specificity

A

proportion of subjects without disease who test negative

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10
Q

define odds ratio

  • odds ratio >1 =
  • odds ratio <1 =
  • Odds ratio = 1

how to calculate odds ratio

A

ratio of the odds that cases were exposed to the odds that controls were exposed

  • Odds ratio >1 = harmful
  • Odds ratio <1 = protective
  • Odd ratio = 1 = no association

(ad)/(bc)

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11
Q

Mineralization:

Osteoid-matrix

  • Collagen, glycoprotein, proteoglycan

Mineralizes to bone

Osteoblasts–>________

Connections: canaliculi

Blood vessels in Haversian canals

Resorption by ________

  • Howship’s lacunae
A

osteocytes

osteoclasts

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12
Q

Regulation of Bone

Periods of __________ and resorption

Mediated by signal molecules

  • Cytokines
  • Growth hormones
  • Inflammation

Receptors on bone cells

Homeostasis - _________

A

formation

dynamic

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13
Q

Histopathology of Periodontal Disease

_________ Gingivitis

Clinical Gingivitis

Periodontitis

A

subclinical

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14
Q

Subclinical Gingivitis

Appears _______

Slight increase in inflammatory cells

  • __________

Limited loss of sulcular ct

A

healthy

neutrophils

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15
Q

Clinical Gingivitis

________, Swelling, small gingival pocket

Proliferating ________ epithelium

Neutrophils in sulcus

Inflammatory cells in ct: PMN, lymphos

A

bleeding

junctional

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16
Q

Periodontitis

Pocket formation

_______ migration of junctional epithelium

Bleeding, Swelling

Anaerobic environment

Inflammatory cells in ct

  • PMN, Lymphocyte, Macrophage, Plasma cells
  • Increased cytokine production

_________ loss

A

Apical

Bone

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17
Q

Cells of the Immune System

_____________

  • Specificity
  • Memory

Antigen Presenting Cells

  • ___________
  • B-lymphocytes
A

lymphocytes

macrophage

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18
Q

Cells of the Immune System (cont.)

Lymphocytes

________ –> bone marrow –> plasma cells –> antibody

_______ —> thymus

  • _______ T cells – Th (CD4+)
  • Cytotoxic T cells – Tc (CD8+) [Suppressors (Ts)]
A

B cells

T cells

Helper

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19
Q

Cells of the Immune System (cont.)

Professional Phagocytes

  • ___________
  • __________ (PMNs)

Auxillary Cells

  • Mast cells
  • Basophils
  • Eosinophils
  • Platelets
A

macrophages

neutrophils

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20
Q

Regulatory Cell Surface Markers

___________

______ (cluster of differentiation)

Cell surface receptors

Adhesins

A

MHC (major histability complex)

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21
Q

Regulatory Cell Surface Markers (cont.)

MHC

  • Foreign graft ________ (i.e. kidney transplant)
  • Introduce foreign antigens to T cells
  • In humans: HLA (human leukocyte antigen)
  • Two major classes:
    • ________ and _______-
A

rejection

clas I and II

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22
Q

Regulatory Cell Surface Markers (cont.)

Physiologic function of MHC molecules

  • Presents antigens to ______
  • Allows recognition of foreignness
A

T cells

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23
Q

Regulatory Cell Surface Markers (cont. )

CD Antigens Differentiate leukocyte populations

  • CD2, CD3 – all T cells
  • _____ – Th cells
  • _____ – Tc/Ts cells
  • CD14 – macrophage
  • CD19 – B cells
A

CD4

CD8

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24
Q

Regulatory Cell Surface Markers (cont. )

Cell Surface Receptors Bind molecules (ligands) and induce growth or secretion

  • _____________
  • Receptors for cytokines
  • Immunoglobulin receptors
  • Complement receptors
A

T cell receptor

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25
Q

Adhesins

  • Bind cells to ________ or to ________

Integrins–on lymphocytes (LFA-1, binds ICAM-1)

Selectins–endothelium (ELAM)

A

each other

tissue

26
Q

Effector Molecules

Products of immune cells which eliminate foreign material

  • __________
  • __________
  • __________
  • Growth Factors
  • Other mediators
A

Immunoglobulins

Complement

Cytokines

27
Q

Effector Molecules (cont.)

Immunoglobulins

  • Produced by ________ cells
  • Five classes
  • _____ – pentameric, first Ab produced
  • IgG – most _______ Ab in serum, produced 2nd, crosses placenta
  • IgA – present in serum as monomer, in secretions as _________
  • IgE – activates _____ cells, involved in allergy
  • IgD – present on _______ of naive B cells
A

plasma

IgM

common

dimeric sIgA

mast

surface

28
Q

Effector Molecules

Immunoglobulins (cont.)

Two regions of Ig

  • Fab fragment – binds ______
  • _____ fragment – binds cells and complement
A

antigen

Fc

29
Q

The Complement System

  • Controls __________ reactions
  • Destroys bacteria
  • Prepares microbes and foreign particles for __________
A

inflammatory

phagocytosis

30
Q

Effector Molecules

The Complement System (cont.)

  • Two pathways of activation
    • ________ – activated by antigen-antibody complexes
      • Components include C1, C4, C2
    • Alternative – activated by _______ molecules (LPS)
      • Components include Factors B and D
A

classical

surface

31
Q

Effector Molecules

The Complement System (cont.)

  • Lytic pathway
    • Cleavage of C3, C5, and formation of _____________
    • Release of C3a and C5a – _________, anaphylactic
    • MAC – C56789 inserts into cell and makes holes
A

membrane attack complex

chemotactic

32
Q

Effector Molecules (cont.)

Cytokines and Their Receptors

  • Chemicals made by immune cells
  • Active at very _____ concentration
  • Can function in autocrine (on self), _____ (nearby cells), or endocrine (systemic) manner
  • Interact with highly sensitive receptors on cells
A

low

paracrine

33
Q

Effector Molecules (cont.)

Growth factors

  • Can promote growth of tissues and block ___________
    • Ex.: Transforming growth factors (i.e. TGF-beta)
A

breakdown

34
Q

Effector Molecules (cont.)

Other Mediators

  • Proteins (i.e. heparin–thins blood)
  • Peptides (i.e. bradykinin–pain sensation)
  • Prostaglandins (i.e. ______-promotes bone loss)
  • Amines (i.e. _______–dilates vessels, contricts airway)
A

PGE2

histamine

35
Q

Innate Immunity

Natural resistance to infection

Activated _________ by pathogens

__________

Cells – neutrophils and macrophages

Effector molecules – complement, cytokines, prostaglandins

A

immediately

nonspecific

36
Q

Conclusions

The patient’s _________ to infections are complex.

The net effect is that the host usually _______ and the infection is controlled.

However, there may be considerable loss of the infected/inflamed tissue.

A

responses

survives

37
Q

Conclusions (cont.)

Bacteria trigger _________ host responses which lead to tissue destruction.

Tissue products such as collagenase, _________, prostaglandins, antibodies, and complement all provide the basis for diagnostic indicator tests.

A

inflammatory

cytokines

38
Q

Conclusions (cont.)

The neutrophil/antibody/complement system is critical for _________ against disease

Tests for neutrophil function, antibody production, and complement opsonization can help identify patients who are ________ for inflammatory diseases.

A

protection

susceptible

39
Q

Conclusions (cont.)

Measurement of factors responsible for healing, such as growth factors, may indicate patients who are _______ to inflammatory diseases.

A

resistant

40
Q

Conclusions (cont.)

________ factors may also play a role in inflammatory disease susceptibility.

HLA typing, chemotactic _________, adhesin abnormalities can be used as indicators of susceptibility

A

genetic

defects

41
Q

Understanding the host response in inflammatory diseases can provide diagnostic ______ as well as better, more specific _______ for patients

A

tools

treatments

42
Q

Innate Immunity in Periodontal Diseases

Activation and emigration of _____ to site of infection

Invading bacteria recognized by _______

  • Release cytokines
    • Recruit WBC
  • Release of enzymes and reactive oxygen
  • Kill bacteria, also destroy tissue
A

PMN

macrophage

43
Q

Host Response in Periodontal Diseases

Immune cell response in periodontitis patients

  • Th:Ts ratio is increased/decreased
  • Regulation of immune response in found in pocket:
    • CD4-Th cells help antibody production
    • CD8-Ts cells suppress antibody production
A

decreased

44
Q

Host Response in Periodontal Diseases: Immune cell response (cont.)

Patient WBC proliferate rapidly to perio ___________

Patients have depressed spontaneous WBC proliferation

  • Improves after treatment (caused by bacteria)
A

bacteria

45
Q

Host Response in Periodontal Diseases

Inflammatory cell response

  • Patient monocytes are hyperreactive to ______
    • Make cytokines (IL-1) and prostaglandins (PGE2 )
    • Possible risk factor?
A

LPS

46
Q

Host Response in Periodontal Diseases

Patients with genetic _________ defects have severe periodontitis

  • Ex.: Agranulocytosis, Cyclic neutropenia

Patients with systemic disease that suppresses neutrophils can have severe periodontitis

  • Ex.: _________, Down’s syndrome, AIDS
A

PMN

diabetes

47
Q

Inflammatory cell response (cont.)

Otherwise healthy patients with depressed PMN’s

  • __________________
  • __________________
  • Refractory periodontitis

Depressed PMN may be caused by bacteria (A.a.) or stress

A

Localized agressive periodontitis (LAP)

Acute necrotizing ulcerative gingivitis (NUG)

48
Q

Regulatory Surface Molecules in Periodontal Disease

______ association with disease

Cell surface receptors

Adhesin abnormalities

A

HLA (human leukocyte antigens)

49
Q

Regulatory Surface Molecules in Periodontal Disease (cont.)

HLA association with disease

  • Certain HLA types more __________ or resistant to disease

Cell surface receptors

  • Neutrophil _________ defect in periodontitis
A

susceptible

chemotactic

50
Q

The Role of Effector Molecules in Periodontal Disease

  • __________
  • Cytokines
  • Prostaglandins
  • __________
  • Complement
A

antibodies

collagenase

51
Q

Effector Molecules (cont.)

Antibodies in Periodontal Disease

  • Adult periodontitis patients
    • Antibodies to P. gingivalis in blood and gingival crevicular fluid (______), elevated IgG4
  • Localized juvenile periodontitis patients A
    • Antibodies to A.a. in blood and GCF, elevated IgG2

Possible blood or GCF ______ for disease

A

GCF
tests

52
Q

Effector Molecules

Antibodies in Periodontal Disease (cont.)

  • Antibodies are generally ________
  • AIDS patients can have severe periodontitis
  • Antibodies can block ________ of bacteria
  • sIgA in saliva can bind bacteria
  • block adherence in pocket

Possible saliva _____ for disease susceptibility

A

protective

colonization

test

53
Q

Effector Molecules (cont.)

The Role of Cytokines in Periodontal Disease

  • IL-1 and TNF found in GCF fluid and tissue in periodontitis
  • Decreased in healthy sites
  • Promotes inflammation and bone __________, activates osteoclasts
A

resorption

54
Q

Effector Molecules (cont.)

The Role of Prostaglandins in Periodontitis

  • _______________ found in diseased tissue and GCF
  • Decreased in health
  • Promotes bone resorption, activates osteoclasts
A

Prostaglandin E2 (PGE2)

55
Q

The Role of Prostaglandins in Periodontitis

Patients taking ____________, ibuprofen) – cyclooxygenase inhibitors

  • Decreased prostaglandins
  • Decreased _____ loss
A

NSAIDS

bone

56
Q

Effector Molecules (cont.)

The Role of Collagenase in Periodontitis

  • Collagenase breaks down connective tissue
  • Produced by bacteria (P. gingivalis)
  • Produced by fibroblasts, __________ in inflamed tissue

Possible GCF marker for tissue ______

A

macrophage

breakdown

57
Q

The Role of Complement in Periodontitis

Periodontal bacteria activate complement

______: antigen-antibody complexes activate the classical pathway

Chronic perio disease: bacteria activate the ______ pathway

Decreased complement activation in healthy sites

A

LAP

alternative

58
Q

Stage 1 Periodontitis: Initial periodontitis

early stages of:

develops in response to:

attachment loss at early ages may indicate:

probing for diagnosis of early disease presents challenges due to:

_____ may increase detection

A

attachment loss

persistence of inflammation and biofilm dysbiosis

heightened susceptability

inaccuracy

salivary biomarkers and/or new imaging technology

59
Q

Stage 2 periodontitis: moderate periodontitis

responds well to:

________ plus _______ may guide for more intensive management for specific patients

A

standard periodontal treatment and frequent monitoring

case grade, treatment

60
Q

Stage 3 periodontitis: severe periodontitis

severe periodontitis with potential for:

in the abscence of treatment, _______ may occur

presence of:

complicated by:

A

additional tooth loss

tooth loss

deep periodontal lesions that extend to middle portion of the root

deep intrabony defects, furcation involvement, history of periodontal tooth loss and ridge defects

61
Q

Stage 4 periodontitis

_______ periodontitis with ______ and potential for ______

considerable damage to:

prescence of:

frequent _____ due to:

A

advanced, extensive tooth loss, loss of dentition

periodontal support

deep periodontal lesions and/or history of multiple tooth loss

hypermobility due to secondary occlusal trauma

62
Q
A

Periodontics (5 decks)

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