FPC2 Perio Exam (Dr. Sun
1. What is the "Non-Specific plaque hypothesis"?: This hypothesis states that all bacteria in plaque contribute to tissue
destruction.
2. What is the "Specific plaque hypothesis?": This hypothesis states that there is a consistent association between
specific bacterial species and clinical disease parameters
3. What is gingivitis?: -Inflammation of the gingiva only
-Direct immune response to the dental microbial plaque building up on teeth
-Modified by several factors (smoking, hormonal changes)
4. What is considered a prerequisite for periodonititis?: Pathogenic biofilm is considered a prerequisite
*This alone is insufficient to cause the disease
5. Does all gingivitis progress to periodontitis?: NO! Gingivitis must precede periodontitis, but not all gingivitis
turns into periodontitis
6. Why is periodontitis variable?: Not all teeth are affected the same The effects can vary from
person to person
Site predilection
7. What is dysbiosis?: Changes in the ecologic balance of the microbiota lead to changes in the bacteria diversity
8. What can dysbiosis cause?: -Overgrowth of potentially pathogenic bacteria
-Loss of bacterial species that are normally beneficial to the host
9. Wha bacteria are found in the Red Biofilm Species Complex?: P. gingivalis
T. forsythensis
T. Denticola
10.What does the the term "virulence factors" refer to?: It refers to all mecha- nisms that enable bacteria to
colonize and damage the tissues of periodontium
11.What are examples of virulence factors?: -Lipopolysaccharides (LPS)
-The ability to invade tissues
-The ability to produce enzymes
12.What is the mechanism of lipopolysaccharides as a virulence factor?: This is detected in the gingival fluid
(GCF) and bears a direct relationship to the degree of inflammation -----> this will cause activation of the complement
pathway
13.Which bacteria have the ability to invade gingival tissues?: P. gingivalis has the ability to penetrate connective
tissues which makes it more difficult to eliminate them through debridement
14.What enzymes can bacteria produce as a virulence factor?: -Collagenases
-Proteases
*These enzymes destory the periodontium
, FPC2 Perio Exam (Dr. Sun
15.In the Tea Laborers in Sri Lanka, what percentage had RAPID progression of interproximal CAL?: 8%
0.1-1 mm lost annually
16. In the Tea Laborers in Sri Lanka, what percentage had MODERATE progres- sion of interproximal
CAL?: 81%
0.05-.5 mm lost annually
17.In the Tea Laborers in Sri Lanka, what percentage had SLOW progression of interproximal CAL?: 11%
0.05-0.09 lost annually
18.What are GENETIC FACTORS that can increase the host's susceptibility of periodontal diseases?: Genes
controlling the formation of biochemical mediators
19.What are the ENVIRONMENTAL FACTORS that can increase the host's susceptibility of periodontal
diseases?: -Tobacco smoking is a known risk factor for periodontal diseases, it has a significant effect on the immune &
and inflammatory systems.
--> impairs neutrophil function, decrease vascularity, and microbial shift to pathologic bacteria
20.What are ACQUIRED FACTORS that can increase the host's susceptibility of periodontal diseases?:
Diabetes is a well-established risk factor for periodontal disease
-->decreases PMN and impairs function, increases cytokine levels (TNF-±,IL-1b), and PGE levels
21.What are the 3 mediators of importance in periodontitis?: -Cytokines
-Prostaglandins
-Matrix Metalloproteinases
22.What TYPE of cytokines are involved with periodontal disease?: -Interleukin 1 (IL-1B)
-Tumor Necrosis Factor-± T( NF-±)
-Interleukin 6 (IL-6)
23. What is the host immune response to CYTOKINES in periodontal disease?-
: -Recruits cells (PMN & macrophages) to the infection site
-Increase vascular permeability, increase movement of immune cells to the site of infection
-Initiates tissue destruction & bone loss
, FPC2 Perio Exam (Dr. Sun
24.What is the host immune response to PROSTAGLANDINS in periodontal disease?: -Increase redness and
tissue edema
-Trigger osteoclastic activity leading to alveolar bone desruction
25.What TYPE of prostaglandins are involved with periodontal disease?: -
-Prostaglandin 1 (PGE 1)
-Prostaglandin 2 (PGE 2)
26.What is the host immune response to MATRIX METALLOPROTEINASES in periodontal disease?: -In
inflammation, overproduction of MMP's leads to exten- sive collagen destruction of the periodontium, this causes pocket
formation, more bacteria, and more inflammation
27.What are the characteristics of the initial lesion stage of periodontitis?: -
-Bacteria colonize near the gingival margin, now virulence factors initiate the host response
-Epithelial cells release TNF-±,MMP, and PGE
-Vasculitis of vessels below JE
-Exudation of fluid into tissues
-Increased migration of leukocytes in JE and sulcus
-Alteration of the most coronal portion of the JE
-Loss of perivascular collagen
28.Is the initial lesion stage of periodontal disease clinically detectable?: NO! this stage is not clinically detectable.
29.What are the characteristics of the early lesion stage of periodontitis?: -
-Bacteria penetrate connective tissue
-More PMN are attracted to the site, and more cytokines come causing more localized destruction of connective tissue
-Accumulation of lymphoid cells immediately below JE
-Further loss of collagen fiber network
1. What is the "Non-Specific plaque hypothesis"?: This hypothesis states that all bacteria in plaque contribute to tissue
destruction.
2. What is the "Specific plaque hypothesis?": This hypothesis states that there is a consistent association between
specific bacterial species and clinical disease parameters
3. What is gingivitis?: -Inflammation of the gingiva only
-Direct immune response to the dental microbial plaque building up on teeth
-Modified by several factors (smoking, hormonal changes)
4. What is considered a prerequisite for periodonititis?: Pathogenic biofilm is considered a prerequisite
*This alone is insufficient to cause the disease
5. Does all gingivitis progress to periodontitis?: NO! Gingivitis must precede periodontitis, but not all gingivitis
turns into periodontitis
6. Why is periodontitis variable?: Not all teeth are affected the same The effects can vary from
person to person
Site predilection
7. What is dysbiosis?: Changes in the ecologic balance of the microbiota lead to changes in the bacteria diversity
8. What can dysbiosis cause?: -Overgrowth of potentially pathogenic bacteria
-Loss of bacterial species that are normally beneficial to the host
9. Wha bacteria are found in the Red Biofilm Species Complex?: P. gingivalis
T. forsythensis
T. Denticola
10.What does the the term "virulence factors" refer to?: It refers to all mecha- nisms that enable bacteria to
colonize and damage the tissues of periodontium
11.What are examples of virulence factors?: -Lipopolysaccharides (LPS)
-The ability to invade tissues
-The ability to produce enzymes
12.What is the mechanism of lipopolysaccharides as a virulence factor?: This is detected in the gingival fluid
(GCF) and bears a direct relationship to the degree of inflammation -----> this will cause activation of the complement
pathway
13.Which bacteria have the ability to invade gingival tissues?: P. gingivalis has the ability to penetrate connective
tissues which makes it more difficult to eliminate them through debridement
14.What enzymes can bacteria produce as a virulence factor?: -Collagenases
-Proteases
*These enzymes destory the periodontium
, FPC2 Perio Exam (Dr. Sun
15.In the Tea Laborers in Sri Lanka, what percentage had RAPID progression of interproximal CAL?: 8%
0.1-1 mm lost annually
16. In the Tea Laborers in Sri Lanka, what percentage had MODERATE progres- sion of interproximal
CAL?: 81%
0.05-.5 mm lost annually
17.In the Tea Laborers in Sri Lanka, what percentage had SLOW progression of interproximal CAL?: 11%
0.05-0.09 lost annually
18.What are GENETIC FACTORS that can increase the host's susceptibility of periodontal diseases?: Genes
controlling the formation of biochemical mediators
19.What are the ENVIRONMENTAL FACTORS that can increase the host's susceptibility of periodontal
diseases?: -Tobacco smoking is a known risk factor for periodontal diseases, it has a significant effect on the immune &
and inflammatory systems.
--> impairs neutrophil function, decrease vascularity, and microbial shift to pathologic bacteria
20.What are ACQUIRED FACTORS that can increase the host's susceptibility of periodontal diseases?:
Diabetes is a well-established risk factor for periodontal disease
-->decreases PMN and impairs function, increases cytokine levels (TNF-±,IL-1b), and PGE levels
21.What are the 3 mediators of importance in periodontitis?: -Cytokines
-Prostaglandins
-Matrix Metalloproteinases
22.What TYPE of cytokines are involved with periodontal disease?: -Interleukin 1 (IL-1B)
-Tumor Necrosis Factor-± T( NF-±)
-Interleukin 6 (IL-6)
23. What is the host immune response to CYTOKINES in periodontal disease?-
: -Recruits cells (PMN & macrophages) to the infection site
-Increase vascular permeability, increase movement of immune cells to the site of infection
-Initiates tissue destruction & bone loss
, FPC2 Perio Exam (Dr. Sun
24.What is the host immune response to PROSTAGLANDINS in periodontal disease?: -Increase redness and
tissue edema
-Trigger osteoclastic activity leading to alveolar bone desruction
25.What TYPE of prostaglandins are involved with periodontal disease?: -
-Prostaglandin 1 (PGE 1)
-Prostaglandin 2 (PGE 2)
26.What is the host immune response to MATRIX METALLOPROTEINASES in periodontal disease?: -In
inflammation, overproduction of MMP's leads to exten- sive collagen destruction of the periodontium, this causes pocket
formation, more bacteria, and more inflammation
27.What are the characteristics of the initial lesion stage of periodontitis?: -
-Bacteria colonize near the gingival margin, now virulence factors initiate the host response
-Epithelial cells release TNF-±,MMP, and PGE
-Vasculitis of vessels below JE
-Exudation of fluid into tissues
-Increased migration of leukocytes in JE and sulcus
-Alteration of the most coronal portion of the JE
-Loss of perivascular collagen
28.Is the initial lesion stage of periodontal disease clinically detectable?: NO! this stage is not clinically detectable.
29.What are the characteristics of the early lesion stage of periodontitis?: -
-Bacteria penetrate connective tissue
-More PMN are attracted to the site, and more cytokines come causing more localized destruction of connective tissue
-Accumulation of lymphoid cells immediately below JE
-Further loss of collagen fiber network
