Pathogenesis of Periodontal Disease Part 2 Flashcards
(45 cards)
1
Q
Eubiosis vs Dysbiosis
A
- Eubiosis: state of balance and health within a microbiome
- Dysbiosis: state of imbalance between microbiomes within the body
2
Q
what is eubiosis in clinically healthy gingival tissue?
A
- plaque is regularly removed and does not accumulate for long on the tooth surface
- small number of neutrophils present in the sulcus
3
Q
What are the stages in the pathogenesis of periodontitis?
A
- Healthy Gingiva: No inflammation, normal tissue architecture.
- Mild Gingivitis (Early Lesion): Develops after 1 week of plaque accumulation; mainly lymphocytes and neutrophils infiltrate.
- Severe Gingivitis (Established Lesion): Chronic inflammation with plasma cells and collagen breakdown.
- Periodontitis (Advanced Lesion): Alveolar bone resorption, deep periodontal pockets, apical migration of junctional epithelium.
4
Q
what are the histological features of clinically healthy gingiva?
A
- CT contains small amount of inflammatory cells (mainly neutrophils)
- neutrophils migrate from CT –> junctional epithelium –> sulcus
- gingival fluid constantly flows from gingival tissue –> gingival crevice
5
Q
What characterizes the Initial Lesion in gingival health?
A
- develops 2 to 4 days after plaque accumulation
- bacterial products activate resident leukocytes, stimulating endothelial cells
- blood capillaries in the gingival connective tissue dilate, increasing vascular permeability, and gingival crevicular fluid flows out of the sulcus
6
Q
How does chemotaxis contribute to neutrophil migration in gingival inflammation?
A
Chemotactic gradients of IL-8 and ICAM-1 direct neutrophils from the vasculature into tissues, guiding them toward the Junctional Epithelium (JE)
7
Q
What molecules are involved in neutrophil activation and migration during inflammation?
A
- LFA-1 (lymphocyte function-associated antigen-1): An integrin receptor aiding in adhesion and migration
- ICAM-1, E-selectin, VCAM: Adhesion molecules expressed by endothelial cells during inflammation
- ICAM-1 and LFA-1 interaction: Allows leukocytes to bind to endothelial cells and transmigrate into tissues
8
Q
What is the process of neutrophils migrating into the Junctional Epithelium (JE)?
A
Neutrophils pass through the basement membrane and enter the JE, moving through intercellular spaces into the gingival sulcus, responding to infection
9
Q
How does the Initial Lesion progress if local factors persist?
A
- If local factors are eliminated, vascular changes resolve, and tissue returns to normal
- If local factors remain or there is a hyperactive host response, the Initial Lesion progresses to the Early Lesion stage
10
Q
What changes occur due to continued plaque accumulation (dysbiosis)?
A
- Increased levels of antigens (bacteria, LPS, etc.)
- Enhanced migration of neutrophils and monocytes
- Vasodilation and elevated vascular permeability
- Edema and erythema of gingival tissues
11
Q
What characterizes the Early Lesion (Mild Gingivitis) after 1 week of plaque accumulation?
A
- Proliferation of capillaries, increased vascular permeability, vasodilation, and gingival crevicular fluid flow
- Large numbers of infiltrating leukocytes (neutrophils and lymphocytes)
- In gingival connective tissue (C.T.): 75% are lymphocytes, mainly T-cells
- In JE and gingival sulcus: mainly neutrophils
12
Q
What tissue changes occur during the Early Lesion phase of gingivitis?
A
- Degeneration of fibroblasts (mainly by apoptosis)
- Collagen destruction leading to collagen-depleted areas
- Proliferation of junctional and sulcular epithelium into the depleted regions
13
Q
What are the possible outcomes for the Early Lesion in gingivitis?
A
- If local factors are eliminated: Vascular changes resolve, tissue reverts to normal, and lost fibers are replaced.
- If local factors remain, abnormal host response, or risk factors persist: Progression to Established Lesion.
14
Q
What defines the Established Lesion phase in gingivitis?
A
- Occurs 2 to 3 weeks after plaque buildup
- Dense inflammatory cell infiltrate (plasma cells, lymphocytes, neutrophils)
- Inflammatory cells accumulate in connective tissues, especially plasma cells and B lymphocytes, surrounding the junctional epithelium, blood vessels, and between collagen bundles
15
Q
What tissue changes occur during the Established Lesion stage?
A
- Release of matrix metalloproteinases and lysosomal enzymes from neutrophils, causing collagen and ground substance destruction
- Significant collagen depletion and proliferation of pocket epithelium with neutrophil accumulation
- Pocket epithelium becomes ulcerated, leading to low resistance to probing and frequent bleeding
16
Q
What are the possible outcomes of the Established Lesion?
A
- Stability: The lesion remains unchanged for months or years.
- Progression: Advances to an Advanced Lesion due to factors like biofilm composition, host immune response, and local/systemic risk factors.
17
Q
What are the primary functions of neutrophils in the gingival environment?
A
- Act as primary mediators of the innate host defense
- Phagocytose and kill bacteria
- Release lysosomal enzymes, cytokines, and reactive oxygen species (ROS) extracellularly
- Form a defense barrier between the subgingival biofilm and gingival tissue in the JE
18
Q
What roles do neutrophils play in maintaining periodontal health?
A
- Protective Role: Phagocytose and kill bacteria, preventing infection. Deficiencies in neutrophil function can lead to susceptibility to infections and severe periodontitis.
- Destructive Role: Release enzymes (e.g., MMPs) during tissue migration, causing breakdown of periodontal structures and collagen depletion. Cytokines and ROS further contribute to tissue damage.
19
Q
What are the key features of continued gingival inflammation?
A
- Fibroblasts degenerate – leading to reduced connective tissue maintenance.
- Collagen destruction – ongoing breakdown and depletion from adjacent tissue, weakening the structural integrity of the gingiva.
20
Q
How does the gingival epithelium respond to collagen depletion during inflammation?
A
- basal cells of the gingival epithelium proliferate into collagen-depleted areas of the connective tissue.
- proliferation acts as a barrier against bacterial invasion and their toxic products, attempting to protect deeper tissues.
21
Q
What are the initial signs of gingival inflammation?
A
- gingival margin becomes edematous (swollen) and slightly enlarged.
- gingival sulcus deepens as inflammation progresses.
- Subgingival biofilm proliferates apically, making plaque control more challenging.
- anaerobic environment of the deepened sulcus supports pathogenic bacterial growth, furthering tissue damage.
22
Q
What are the possible progressions of an Established Lesion?
A
- Remain Stable: Does not progress for months or even years.
- Progress to Advanced Lesion: Influenced by: Microbial biofilm composition and quantity, Host immune and inflammatory response, Local and systemic risk factors
23
Q
What are the main features of the Advanced Lesion in periodontitis?
A
- Dominance of neutrophils in pocket epithelium and periodontal pockets.
- Dense infiltration of plasma cells in gingival connective tissue.
- Significant collagen breakdown, resulting in large areas of depleted connective tissue.
- Apical migration of the junctional epithelium to maintain barrier integrity.
- Alveolar bone resorption by osteoclasts, with plaque bacteria proliferating apically.
24
Q
What is the difference between a gingival sulcus and a periodontal pocket?
A
- Gingival Sulcus: The natural space between the tooth and surrounding gingival tissue in healthy conditions.
- Periodontal Pocket: A pathologically deepened gingival sulcus caused by disease processes
25
What is a pseudopocket and how does it form?
- enlarged gingival sulcus formed by the coronal advancement of the gingival margin due to inflammation or enlargement.
*There is no attachment loss or alveolar bone loss, distinguishing it from a true periodontal pocket
26
What characterizes a periodontal pocket?
- pathological deepening of the gingival sulcus due to coronal advancement of the gingival margin and apical displacement of the epithelial attachment.
*It is marked by loss of attachment and often followed by alveolar bone loss
27
What are the two main types of periodontal pockets?
- Suprabony Pocket: Located coronal to the level of the adjacent alveolar bone.
- Intrabony Pocket: Positioned apical to the level of the adjacent alveolar bone.
28
What microbial features are associated with periodontal pockets?
- various microbial species that thrive in the local environment.
- pocket favors certain microorganisms due to specific conditions (e.g., oxygen levels, nutrients).
- Unique aspect: The tooth surface serves as a distinct environment for microbial colonization.
29
What causes the destruction of collagen fibers in gingival connective tissue?
Destruction is primarily caused by matrix metalloproteinases (MMPs) released by resident and inflammatory cells and the main contributing cells include:
- Fibroblasts
- Neutrophils
- Macrophages
30
What happens if the bacterial infection persists in periodontal disease?
- Leukocyte migration and release of inflammatory mediators and destructive enzymes escalate that leads to increased connective tissue breakdown.
- junctional epithelium (JE) and pocket epithelium thin out, ulcerate, and bleed more easily during probing
31
How does the junctional epithelium (JE) migrate during periodontal disease progression?
- Cells at the coronal aspect detach from the root surface
- Cells at the apical aspect migrate apically into collagen-depleted areas.
- Intraepithelial clefts form, leading to epithelial proliferation and thickening, which reduces nutrient supply and can cause necrosis.
32
What causes the coronal portion of the junctional epithelium (JE) to detach from the tooth surface?
- Neutrophils migrate from connective tissue (C.T.) into the JE
- Migration increases during the Advanced Lesion stage.
- When neutrophils reach about 60% of the JE, epithelial cells lose cohesiveness, causing the coronal portion to detach from the tooth
33
What are the steps that lead to the development of a periodontal pocket?
1. Dental plaque accumulation
2. Gingival inflammation (vasodilation, edema, inflammatory cell migration)
3. Collagen fiber destruction (apical and lateral to the JE)
4. Apical proliferation of JE cells along the root surface
5. Coronal detachment of the JE from the root surface
6. Oral sulcular epithelium gradually replaces the pocket wall
34
What are the key features of the junctional epithelium in a healthy state?
- Functions as a barrier against plaque bacteria
- stratified squamous nonkeratinized epithelium
- Apical portion usually on enamel
- Attached to the tooth by internal basal lamina and to C.T. by external basal lamina
- high permeability for cells and fluids
- high rates of cellular proliferation and turnover
35
How does the JE change in inflamed periodontal tissue?
- Becomes shorter than in healthy tissue
- Apical portion moves to the root surface
- Infiltrated by inflammatory cells (mainly neutrophils)
- Cells show degeneration and ulceration
- Less resistant to probing, increasing bleeding risk
36
What changes occur in the epithelium of the lateral wall of a periodontal pocket?
- Infiltration by leukocytes and edema from inflamed connective tissue
- Formation of epithelial buds projecting into inflamed tissue
- Degeneration and necrosis can lead to ulceration and exposure of underlying tissue
37
What are some unique features of the epithelial part of the pocket wall?
- No direct correlation between pocket depth and degenerative severity
- At the gingival crest, epithelium is intact, thickened, and has prominent rete pegs
- More pronounced degeneration in aggressive periodontitis compared to nonaggressive forms
38
What changes are seen in the connective tissue of a periodontal pocket wall?
- Increased blood vessels and endothelial cell proliferation
- Dilated capillaries and edematous tissue
- Infiltration with plasma cells (80%) and lymphocytes
- Degeneration of fibroblasts and destruction of gingival fibers
- Presence of newly formed fibroblasts and collagen fibers
39
What is the surface morphology of the tooth wall in a periodontal pocket?
1. Cementum covered by calculus
2. Attached plaque covers calculus and extends apically
3. Unattached plaque surrounds the attached plaque and extends apically
4. Junctional epithelium is <100 µm thick, versus >500 µm in normal sulcus
5. Partially destroyed CT fibers
6. Intact CT fibers
40
Can periodontal pockets resolve without treatment?
yes, pockets undergo tissue destruction and repair cycles where granulation tissue forms with fibroblasts, keratinocytes, and new capillaries.
***Complete healing does not occur if infectious factors are still present.
41
What pathological changes happen to the root surface of a periodontal pocket?
- Collagen fibers (Sharpey's fibers) undergo destruction and degeneration.
- Cementum becomes exposed, allowing bacteria to penetrate.
- Bacterial invasion leads to further cementum breakdown.
42
How do bacteria penetrate the root cementum in periodontal disease?
Bacteria may reach the cemento-dentinal junction and dentinal tubules and cause fragmentation of the cementum surface, leading to necrosis (87% of periodontally diseased teeth)
**Endotoxins can prevent fibroblast attachment, hindering healing.
43
What triggers alveolar bone loss in periodontal disease?
- Triggered by inflammatory mediators in gingival tissue and activation of inflammatory pathways leads to bone resorption
**Mediators must reach a critical distance to the alveolar bone to initiate loss.
44
Describe the multistep process of alveolar bone loss.
1. Proliferation of osteoclast precursors (progenitor cells, macrophages).
2. Commitment of these precursors to the osteoclast phenotype.
3. Degradation of bone's organic and inorganic matrix by osteoclasts.
4. Process is driven by proinflammatory cytokines (IL-1β, TNF-α, IL-6).
45
How is bone loss controlled during inflammation?
- Controlled by the RANK/RANKL/OPG mechanism where RANKL binds to RANK on osteoclast precursors, activating them.
- OPG (osteoprotegerin) acts as a decoy receptor, preventing RANKL from binding to RANK, inhibiting osteoclast activation.
