Etiology and Pathogenesis of Periodontal Disease Flashcards
1
Q
What is the etiologic factor of Periodontal Disease?
A
PLAQUE
2
Q
Define gingivitis?
A
An inflammatory process confined to the gingival tissues
3
Q
Is gingivitis reversible?
A
Yes, usually.
4
Q
Define periodontitis?
A
Inflammation not confined to the gingiva, but involves the attachment apparatus (cementum, periodontal ligament, alveolar bone, and soft tissue)
5
Q
Where does periodontal disease stem from?
A
Microbial plaque
Genetics/Host Factors
Acquired/Environmental Factors
6
Q
What are Koch’s postulates?
A
1) Microbe must be present in all cases
2) Microbe must then be isolated and grown
3) Microbe must cause same disease in another animal
4) Microbe must be reisolated and prove to be the original microbe
7
Q
Based off the Danish study, how long does it take to develop gingivitis?
A
10-21 days
8
Q
Based off the Danish study, how long did it take for people who had gingivitis to recover with oral hygiene?
A
1 week
9
Q
Based off the Danish study, the appearance of gram negative flora preceded detectable gingivitis by how many days?
A
3-10 days
10
Q
In what layers do bacteria grow?
A
aerobic -> facultative -> anaerobic
11
Q
What hypothesis is believed to be the etiology of periodontal disease?
A
Specific plaque hypothesis combined with a susceptible host.
1) Bacterial infections
2) Risk factors
3) Systemic effects
12
Q
What bacterial enzymes are known to cause tissue destruction?
A
Collagenase Proteases Nueraminidase Ribonuclease Deoxyribonuclease Hyaluronidase Chondroitin sulfatase
13
Q
What bacterial cytotoxic agents cause cell death?
A
Exotoxin of actinobacillus Endotoxin (gram negative) Mucopeptides (gram positive) Ammonia Hydrogen Sulfide Toxic amines Organic acids
14
Q
What did the sri lanka data?
A
Not all individuals get periodontitis
15
Q
What microbes make up microbial plaque?
A
Bacteria Fungus Protozoa Virus Mycoplasm
16
Q
What are innate risk factors that lead to periodontal disease?
A
Race Sex Genetic factors/inheritance Congenital immunodeficiencies Phagocytic dysfunction Down syndrome Papillon-Lefevre/Ehlers-Dantos syndrome
17
Q
What are two places calculus attaches to?
A
Supragingival calculus
Subgingival calculus
18
Q
Basic properties of biofilms?
A
Cooperating community
Microcolonies connected with channels
Microcolonies protected with protective matrix
Quorum Sensing
Resistance to antibiotics, immune system, antimicrobials
19
Q
What types of colonizers are there that attach to the pellicle?
A
Early Colononizers
Late Colonizers
20
Q
Which type of colonizers are most likely to cause periodontal diseases?
A
1) Red Complex
- P. gingivalis
- T. forsythensis
- T. denticola
- Aggregatibacter actinomycetemcomitans
2) Orange complex
- Campylobacter: gracili, rectus, showae
- Eubacterium: nodatum
- Fusobacterium: nucleatum, polymorphum
- Prevotella: intermedia, nigrescens
- Peptostreptococcus: micros
- Streptococcus: constellatus
21
Q
What do many of the main late colonizers have in common?
A
gram neg
non-motile
22
Q
What does the fluid gradient in the mouth do to help a biofilm?
A
moves nutrients around
allows bacteria to communicate
23
Q
How can biofilms resist antibiotics?
A
antibiotic penetrates too slowly or incompletely
24
Q
What initiates and progresses periodontal disease?
A
Initiation: non specific plaque accumulation
progression: G- bacteria and susceptible host.
25
Where is plaque most likely to accrue?
Distally, on the buccal posterior teeth
26
T/F Not all gingivitis progresses to periodontitis but all periodontitis is preceded by gingivitis.
T
27
Virulence or pathogenicity factors that enable bacteria to cause disease?
1) fimbrae, pili: allow attachment and prevent phagocytosis
2) Capsule: allows protection, attachment, prevents phagocytosis
3) Endotoxin: activation of inflammatory response, cytokine production, bone resorption
28
T/F The ability for bacteria to adhere is a virulence factor?
T
29
How are bacteria displace if they do not attach to the pellicle?
Due to gingival crevicular fluid
30
What is the formula that adds up to periodontal disease?
Pathogenic flora + Lack of beneficial bacteria + susceptible host
31
What is larger player with a big name known to be a periodontal pathogen?
Aggregatibacter actinomycetemcomitans
32
What are beneficial bacteria in the periodontium?
```
Actinomyces spp.
Strep. mitis
Strep. sanguis
Capnocytophaga spp.
V. parvula
```
33
What are factors that could lead to a susceptible host?
```
Impaired neutrophils
Inadequate immune response
LPS responsiveness
AIDS
Diabetes
Smoking
Drugs
```
34
What are the types of dental plaque?
Supragingival: coronal, marginal
Subgingival: Attached plaque (tooth, epithelium, CT) Unattached
35
What characteristic do unattached plaque usually have?
G-
Motile
Inbetween attached plaque and sulcular epithelium
In contact with junctional and sulcular epithelium
36
Steps of plaque formation?
1) Pellicle formation
2) Attachment
3) Young supra-gingival plaque (G+ mainly)
4) Aged supra-gingival plaque (G- increase)
5) Sub-gingival plaque (attached, unattached)
37
What main difference exist between supra and sub gingival plaque?
Supra: G+ mostly, non-motile mainly, aerobic unless thick, metabolizes carbs
Sub: G- mostly, motile, anaerobic, metabolizes proteins
38
What main differences exist between tooth and epithelium associated subgingival plaque?
Tooth-associated: G+, does not extend to JE, may penetrate cementum, calculus & root caries
Epithelium-associated: G+ & G-, Extends to JE, may penetrate epithelium/CT, gingivitis and periodontitis
39
Bacteria with a very strong association to Periodontal diseases?
A.a.
P. Gingivalis
T. Forsythia
40
Bacteria with a strong association to Periodontal diseases?
```
P. intermedia
E. nodatum
Treponema sp.
Eubacterium sp.
C. rectus
```
41
Bacteria with a moderate association to Periodontal diseases?
S. intermedius
F. nucleatum
E. corrodens
P. Micros
42
Chronic periodontitis commonly involves what bacteria?
```
P. gingivalis
P. intermedia
F. nucleatum
A.a.
C. recta
T. forsythia
```
43
What does LAP stand for?
Localized agressive periodontitis
- A.a.
- P. intermedia
- P. gingivalis
44
Refractory disease is commonly caused by what bacterium?
T. forysthia
P. gingivalis
P. intermedia
C. recta
45
What does NUG stand for?
Necrotizing Ulcerating Gingivitis
- caused by P. intermedia (intermediate sized spirochetes)
46
What are HIV associated bacteria that cause gingivitis?
```
Candida albicans (yeast)
P. gingivalis
P. intermedia
F. nucleatum
A.a.
C. recta
```
47
Describe attributes of Aggregatibacter actinomycetemcomitans?
```
Small, non-motile
G-
Facultative anaerobe
Saccharolytic
Coccobacillus
Prevelance 90% in LAP
Prevelance 30-50% in chronic periodontitis
```
48
What unique ability does Aggregatibacter actinomycetemcomitans to cause serious damage?
* *** has the ability to invade host epithelial cells****
| * *** releases exotoxin called a LEUKOTOXIN
49
What is an endotoxin?
Found in G- bacteria. LPS layer has the ability to release virulent factors into surrounding environment either by cell degradation or by budding off pieces of LPS.
This has cytotoxic effects. Leads to bone resorption.
50
Describe attributes of P. gingivalis?
```
G-
anaerobic
non-motile
Bacillus
Fimbriae
forms dark brown-black colonies
```
51
Describe unique attributes of P. gingivalis?
* *** has the ability to invade host epithelial cells****
* *** able to grow at low pH
* *** has a thick capsule to resist phagocytosis
* *** has proteinases - include collagenase
* *** stimulates cytokine production in monocytes and macrophages
52
Describe attributes of T. forsythia
G-
anerobic
grows best with F. nucleatum
**** invades epithelial cells
53
Describe attributes of P. intermedia
Black pigmented bacteroides
G-
anaerobic
Elevated in ANUG
54
Describe attributes of F. nucleatum
G-
anaerobic
Spindle shaped rod
**** most common isolate from sub-gingival samples
55
Describe attributes of C. rectus
G-
anaerobic
Motile
*** produces leukotoxin
56
Describe attributes of P. micros
G+ (only one in lecture discussed)
anaerobic
small coccus
57
Describe attributes of spirochetes
G-
anaerobic
helical shaped
related to NUG
58
What is considered an active site?
A site that shows attachment loss greater than 2-2.5mm in 2 months.
59
What occurs with initial (2-4 day) lesion?
Histologically: Vasculitis, exudation of fluid from sulcus, inc. in leukocytes into j.e. and sulcus, serum proteins released extrvascularly *fibrin
Clinically: appears healthy
60
What occurs with early lesion (4-7) days?
Histologically: accumulation of lymphoid cells into j.e., fibroblast activation, loss of collagen network of marginal gingiva, proliferation of basal cells of j.e.
Clinically: gingivitis, w/ no change in pp depth or bone loss
61
What occurs with an established lesion (2-3) weeks?
Histologically: acute inflammation, plasma cells present w/o bone loss, immunoglobulins extravascular in CT and j.e., continuation of tissue loss, early pocket formation
Clinically: gingivitis, change in gingiva color, no periodontal pocket or bone loss
62
What occurs with an advance lesion (>3 weeks)?
Histologically: Extension into alveolar bone and PDL, Collagen loss in pocket epithelium continued, periodontal pockets present, quiescence and exacerbation, bone marrow converted into fibrous connective tissue, widespread inflammation
Clinically: Periodontitis, change in color, Periodontal Pocket, Alveolar bone loss on radiographs
63
How does the body heal from periodontal disease?
Bacteria and bacterial products removed by phagocytes
Cytokines aid in repair of tissue and epithelium.
64
What is the bodies immune response to plaque accumulation and initiation of gingivitis?
Mast cells
acute phase proteins
PMNs
Antibodies
65
Events of the inflammatory process?
1) tissue injury --> chemical mediators released to increase permeability of adjacent small blood vessels
2) Blood vessel dilation and inc. permeability --> Tissues swell, Elevated temp, Redness, Pain from pressure in tissues
3) WBC adhere to walls of blood vessels --> chemotaxis of WBC, phagocytosis induced, and Antibody production intiated
66
What do mast cells release during inflammation?
Histamine
Chemotactic factors: eosinophils and PMN can come in
Interleukins
TNF alpha: recruitment of granulocytes --> fever
Leukotrienes: dilation of blood vessels
Protaglandins: inc. vascular permeability
67
Describe acute phase proteins.
```
Plasma proteins increased due to microbial infection
Examples:
C-reactive protein
Fibrinogen
Complement
Mannose-binding protein
Metal-binding proteins
```
68
What is a complement system?
20 different protein molecules always found in the blood. There are no cells in the system. With an infection, this system of molecules is activated, leading to a sequence of events on the surface of the pathogen that helps destroy the pathogen and eliminate the infection.
The complement system can be activated in two main ways. The first means of activation is part of the innate (natural) immune response. (i.e.; neither antibodies nor T cell receptors are involved.) For example, certain polysaccharides found on the surface of bacteria can activate the system. This can occur immediately and does not require prior exposure to the molecules.
The second and most potent means occurs in a adaptive immune response when antibodies (IgG or IgM) binds to antigen at the surface of a cell. This exposes the Fc region of the antibody in a way that allows the first complement protein (C1) to bind.
69
What happens as a result of the activation of a complement system?
A cascade of events follows, in which each step leads to the next. At the center of the cascade are steps in which the proteolysis of a complement protein leads to a smaller protein and a peptides. The smaller protein remains bound to the complex at the surface of the microorganism, while the peptide diffuses away.
Complement C3 is cleaved into C3b and C3a. C3b remains bound to the complex at the surface of the microorganism. This not only activates the next step, but also C3b is a good opsonin. The small peptide, C3a diffuses away and acts as a chemotactic factor and an inflammatory paracrine.
Next, complement protein C5 is cleaved into C5b and C5a. The C5b remains bound to complex on the surface of the cell while the C5a diffuses away and acts much like C3a.
Then the complement proteins C6, C7, and C8 bind successively to the growing complex. Finally, a number of C9 complement proteins bind to the complex. These C9 proteins are elongated molecules that form a circle with a large hole in the middle. This structure, which is called a membrane attack complex (MAC), pierces the membrane of the cell. This initiates a sequence of event leading to lysis (of a microbe) or apoptosis (of a cell of the body in pathologies and tissue transplants).
70
A complement response system aids in carrying out what parts of an immune response?
opsonization (labeling pathogen)
chemotaxis
inflammation
lysis, apoptosis
71
What does a MAC do?
Membrane attack complex: creates a hole in the membrane of the pathogens cell wall.
72
What types of leukocytes are there?
Granulocytes: Neutrophils (aka PMN, most common of all cells), Eosinophils, Basophils
Mononuclear phagocytes: --> monocytes, machrophages, dendritic cells
Lymphocytes: NK cells, T cells, B cells
73
What are characteristic of PMNs?
Terminal cell with short half life
Roll around on endothelium (diapedesis, chemotaxis)
Adhere to target, phagocytize, lyse or apoptose
*****Kill with oxidative or nonoxidative means
74
What stimulates the entrance of PMNs into infected tissue?
Bacterial LPS layers triggers selectins to be released on endothelium
Additionally monocyte releases IL-1 or TNF-alpha which causes selectins to be released on endothelium
Then Integrins are expressed on endothelium and PMN enters
75
What is the most common bacterial protein that the body detects to initiate an immune response?
F-met peptides
76
What are common everyday host risk factors can modify neutrophils ability to be effective?
Diabetes
| Smoking
