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
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
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
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
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
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
7
Q
pandemic
A
worldwide epidemic
8
Q
sensitivity
A
proportion of subjects with disease who test positive
9
Q
Specificity
A
proportion of subjects without disease who test negative
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)
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
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
13
Q
Histopathology of Periodontal Disease
_________ Gingivitis
Clinical Gingivitis
Periodontitis
A
subclinical
14
Q
Subclinical Gingivitis
Appears _______
Slight increase in inflammatory cells
- __________
Limited loss of sulcular ct
A
healthy
neutrophils
15
Q
Clinical Gingivitis
________, Swelling, small gingival pocket
Proliferating ________ epithelium
Neutrophils in sulcus
Inflammatory cells in ct: PMN, lymphos
A
bleeding
junctional
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
17
Q
Cells of the Immune System
_____________
- Specificity
- Memory
Antigen Presenting Cells
- ___________
- B-lymphocytes
A
lymphocytes
macrophage
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
19
Q
Cells of the Immune System (cont.)
Professional Phagocytes
- ___________
- __________ (PMNs)
Auxillary Cells
- Mast cells
- Basophils
- Eosinophils
- Platelets
A
macrophages
neutrophils
20
Q
Regulatory Cell Surface Markers
___________
______ (cluster of differentiation)
Cell surface receptors
Adhesins
A
MHC (major histability complex)
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
22
Q
Regulatory Cell Surface Markers (cont.)
Physiologic function of MHC molecules
- Presents antigens to ______
- Allows recognition of foreignness
A
T cells
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
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
25
Adhesins
* Bind cells to ________ or to \_\_\_\_\_\_\_\_
Integrins--on lymphocytes (LFA-1, binds ICAM-1)
Selectins--endothelium (ELAM)
each other
tissue
26
**Effector Molecules**
Products of immune cells which eliminate foreign material
* \_\_\_\_\_\_\_\_\_\_
* \_\_\_\_\_\_\_\_\_\_
* \_\_\_\_\_\_\_\_\_\_
* Growth Factors
* Other mediators
Immunoglobulins
Complement
Cytokines
27
**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
plasma
IgM
common
dimeric sIgA
mast
surface
28
**Effector Molecules**
Immunoglobulins (cont.)
Two regions of Ig
* Fab fragment -- binds \_\_\_\_\_\_
* _____ fragment -- binds cells and complement
antigen
Fc
29
**The Complement System**
* Controls __________ reactions
* Destroys bacteria
* Prepares microbes and foreign particles for \_\_\_\_\_\_\_\_\_\_
inflammatory
phagocytosis
30
**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
classical
surface
31
**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
membrane attack complex
chemotactic
32
**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
low
paracrine
33
**Effector Molecules (cont.)**
Growth factors
* Can promote growth of tissues and block \_\_\_\_\_\_\_\_\_\_\_
* Ex.: Transforming growth factors (i.e. TGF-beta)
breakdown
34
**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)
PGE2
histamine
35
**Innate Immunity**
Natural resistance to infection
Activated _________ by pathogens
\_\_\_\_\_\_\_\_\_\_
Cells -- neutrophils and macrophages
Effector molecules -- complement, cytokines, prostaglandins
immediately
nonspecific
36
**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.
responses
survives
37
**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.
inflammatory
cytokines
38
**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.
protection
susceptible
39
**Conclusions (cont.)**
Measurement of factors responsible for healing, such as growth factors, may indicate patients who are _______ to inflammatory diseases.
resistant
40
**Conclusions (cont.)**
\_\_\_\_\_\_\_\_ factors may also play a role in inflammatory disease susceptibility.
HLA typing, chemotactic \_\_\_\_\_\_\_\_\_, adhesin abnormalities can be used as indicators of susceptibility
genetic
defects
41
Understanding the host response in inflammatory diseases can provide diagnostic ______ as well as better, more specific _______ for patients
tools
treatments
42
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
PMN
macrophage
43
**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
decreased
44
**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)
bacteria
45
**Host Response in Periodontal Diseases**
Inflammatory cell response
* Patient monocytes are hyperreactive to \_\_\_\_\_\_
* Make cytokines (IL-1) and prostaglandins (PGE2 )
* Possible risk factor?
LPS
46
**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
PMN
diabetes
47
**Inflammatory cell response (cont.)**
Otherwise healthy patients with depressed PMN’s
* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* Refractory periodontitis
Depressed PMN may be caused by bacteria (A.a.) or stress
Localized agressive periodontitis (LAP)
Acute necrotizing ulcerative gingivitis (NUG)
48
**Regulatory Surface Molecules in Periodontal Disease**
\_\_\_\_\_\_ association with disease
Cell surface receptors
Adhesin abnormalities
HLA (human leukocyte antigens)
49
**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
susceptible
chemotactic
50
**The Role of Effector Molecules in Periodontal Disease**
* \_\_\_\_\_\_\_\_\_\_
* Cytokines
* Prostaglandins
* \_\_\_\_\_\_\_\_\_\_
* Complement
antibodies
collagenase
51
**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
GCF
tests
52
**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
protective
colonization
test
53
**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
resorption
54
**Effector Molecules (cont.)**
The Role of Prostaglandins in Periodontitis
* _______________ found in diseased tissue and GCF
* Decreased in health
* Promotes bone resorption, activates osteoclasts
Prostaglandin E2 (PGE2)
55
**The Role of Prostaglandins in Periodontitis**
Patients taking \_\_\_\_\_\_\_\_\_\_\_\_, ibuprofen) -- cyclooxygenase inhibitors
* Decreased prostaglandins
* Decreased _____ loss
NSAIDS
bone
56
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 \_\_\_\_\_\_
macrophage
breakdown
57
**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
LAP
alternative
58
**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
attachment loss
persistence of inflammation and biofilm dysbiosis
heightened susceptability
inaccuracy
salivary biomarkers and/or new imaging technology
59
**Stage 2 periodontitis: moderate periodontitis**
responds well to:
\_\_\_\_\_\_\_\_ plus _______ may guide for more intensive management for specific patients
standard periodontal treatment and frequent monitoring
case grade, treatment
60
**Stage 3 periodontitis: severe periodontitis**
severe periodontitis with potential for:
in the abscence of treatment, _______ may occur
presence of:
complicated by:
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
Stage 4 periodontitis
\_\_\_\_\_\_\_ periodontitis with ______ and potential for \_\_\_\_\_\_
considerable damage to:
prescence of:
frequent _____ due to:
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
Periodontics
flashcards
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