Exam 2 Flashcards
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
1) intact
- <10%
- 3mm
- BOP
2) reduced
- stable
- stable non-periodontitis
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?
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
what are the symptoms and findings of necrotizing disease?
NG
NP
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
what is the purpose of staging?
What is the purpose of grading?
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
endemic
examples
habitual presence of a disease within a given geographic area
- Usual occurrence of a given disease within such an area
- Examples: malaria
epidemic
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
pandemic
worldwide epidemic
sensitivity
proportion of subjects with disease who test positive
Specificity
proportion of subjects without disease who test negative
define odds ratio
- odds ratio >1 =
- odds ratio <1 =
- Odds ratio = 1
how to calculate odds ratio
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)
Mineralization:
Osteoid-matrix
- Collagen, glycoprotein, proteoglycan
Mineralizes to bone
Osteoblasts–>________
Connections: canaliculi
Blood vessels in Haversian canals
Resorption by ________
- Howship’s lacunae
osteocytes
osteoclasts
Regulation of Bone
Periods of __________ and resorption
Mediated by signal molecules
- Cytokines
- Growth hormones
- Inflammation
Receptors on bone cells
Homeostasis - _________
formation
dynamic
Histopathology of Periodontal Disease
_________ Gingivitis
Clinical Gingivitis
Periodontitis
subclinical
Subclinical Gingivitis
Appears _______
Slight increase in inflammatory cells
- __________
Limited loss of sulcular ct
healthy
neutrophils
Clinical Gingivitis
________, Swelling, small gingival pocket
Proliferating ________ epithelium
Neutrophils in sulcus
Inflammatory cells in ct: PMN, lymphos
bleeding
junctional
Periodontitis
Pocket formation
_______ migration of junctional epithelium
Bleeding, Swelling
Anaerobic environment
Inflammatory cells in ct
- PMN, Lymphocyte, Macrophage, Plasma cells
- Increased cytokine production
_________ loss
Apical
Bone
Cells of the Immune System
_____________
- Specificity
- Memory
Antigen Presenting Cells
- ___________
- B-lymphocytes
lymphocytes
macrophage
Cells of the Immune System (cont.)
Lymphocytes
________ –> bone marrow –> plasma cells –> antibody
_______ —> thymus
- _______ T cells – Th (CD4+)
- Cytotoxic T cells – Tc (CD8+) [Suppressors (Ts)]
B cells
T cells
Helper
Cells of the Immune System (cont.)
Professional Phagocytes
- ___________
- __________ (PMNs)
Auxillary Cells
- Mast cells
- Basophils
- Eosinophils
- Platelets
macrophages
neutrophils
Regulatory Cell Surface Markers
___________
______ (cluster of differentiation)
Cell surface receptors
Adhesins
MHC (major histability complex)
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 _______-
rejection
clas I and II
Regulatory Cell Surface Markers (cont.)
Physiologic function of MHC molecules
- Presents antigens to ______
- Allows recognition of foreignness
T cells
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
CD4
CD8
Regulatory Cell Surface Markers (cont. )
Cell Surface Receptors Bind molecules (ligands) and induce growth or secretion
- _____________
- Receptors for cytokines
- Immunoglobulin receptors
- Complement receptors
T cell receptor
Adhesins
- Bind cells to ________ or to ________
Integrins–on lymphocytes (LFA-1, binds ICAM-1)
Selectins–endothelium (ELAM)
each other
tissue
Effector Molecules
Products of immune cells which eliminate foreign material
- __________
- __________
- __________
- Growth Factors
- Other mediators
Immunoglobulins
Complement
Cytokines
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
Effector Molecules
Immunoglobulins (cont.)
Two regions of Ig
- Fab fragment – binds ______
- _____ fragment – binds cells and complement
antigen
Fc
The Complement System
- Controls __________ reactions
- Destroys bacteria
- Prepares microbes and foreign particles for __________
inflammatory
phagocytosis
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
- ________ – activated by antigen-antibody complexes
classical
surface
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
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
Effector Molecules (cont.)
Growth factors
- Can promote growth of tissues and block ___________
- Ex.: Transforming growth factors (i.e. TGF-beta)
breakdown
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
Innate Immunity
Natural resistance to infection
Activated _________ by pathogens
__________
Cells – neutrophils and macrophages
Effector molecules – complement, cytokines, prostaglandins
immediately
nonspecific
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
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
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
Conclusions (cont.)
Measurement of factors responsible for healing, such as growth factors, may indicate patients who are _______ to inflammatory diseases.
resistant
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
Understanding the host response in inflammatory diseases can provide diagnostic ______ as well as better, more specific _______ for patients
tools
treatments
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
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
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
Host Response in Periodontal Diseases
Inflammatory cell response
- Patient monocytes are hyperreactive to ______
- Make cytokines (IL-1) and prostaglandins (PGE2 )
- Possible risk factor?
LPS
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
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)
Regulatory Surface Molecules in Periodontal Disease
______ association with disease
Cell surface receptors
Adhesin abnormalities
HLA (human leukocyte antigens)
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
The Role of Effector Molecules in Periodontal Disease
- __________
- Cytokines
- Prostaglandins
- __________
- Complement
antibodies
collagenase
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
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
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
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)
The Role of Prostaglandins in Periodontitis
Patients taking ____________, ibuprofen) – cyclooxygenase inhibitors
- Decreased prostaglandins
- Decreased _____ loss
NSAIDS
bone
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
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
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
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
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
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
