exam review Flashcards
1
Q
What are the four main components of the periodontium?
A
Gingiva, Periodontal Ligament (PDL), Cementum, Alveolar Bone.
2
Q
What are the three divisions of the gingiva?
A
Free gingiva, attached gingiva, interdental gingiva (papilla).
3
Q
What are the clinical features of healthy gingiva?
A
Pink color, keratinized, stippled appearance.
4
Q
What is the main function of the periodontal ligament (PDL)?
A
Shock absorption, proprioception, and maintaining homeostasis.
5
Q
Which PDL fiber group is the most abundant and acts as the primary load absorber?
A
Oblique fibers.
6
Q
What are the two types of cementum, and where are they found?
A
Acellular Cementum: Cervical 2/3 of the root, provides most of the attachment.
Cellular Cementum: Apical 1/3 and furcations, contains cementocytes and adapts to wear.
7
Q
What are the three components of alveolar bone?
A
Alveolar Bone Proper (Lamina Dura), Cortical Bone, Cancellous Bone.
8
Q
What are the three types of gingival epithelium?
A
Oral epithelium, sulcular epithelium, junctional epithelium.
9
Q
Which gingival epithelium type is keratinized?
A
Oral epithelium.
10
Q
What makes junctional epithelium unique?
A
It is non-keratinized, has wider intracellular spaces, and allows immune cell migration.
11
Q
What are the four layers of oral epithelium?
A
Stratum corneum (keratinized layer)
Stratum granulosum (keratohyalin granules)
Stratum spinosum (desmosomes)
Stratum basale (cell renewal)
12
Q
What is the turnover rate of junctional epithelium?
A
4-6 days.
13
Q
What are the three types of non-keratinocytes in gingival epithelium?
A
Melanocytes – produce melanin.
Langerhans cells – antigen-presenting immune cells.
Merkel cells – involved in touch sensation.
14
Q
What is the primary function of collagen in the ECM?
A
Provides tensile strength and structural integrity.
15
Q
What is the role of elastin in the ECM?
A
Contributes to tissue elasticity.
16
Q
What are glycosaminoglycans (GAGs), and what do they do?
A
Linear polysaccharides that maintain tissue hydration and resilience.
17
Q
Which type of collagen is most abundant in the periodontium?
A
Type I collagen.
18
Q
What type of collagen is found in basement membranes?
A
Type IV collagen.
19
Q
What is the role of Connective Tissue Growth Factor (CTGF)?
A
It is an extracellular matrix protein involved in the control of biological processes.
20
Q
What is the function of Transforming Growth Factor Beta (TGF-β)?
A
It is a potent stimulator of collagen production.
21
Q
What are the first two steps of collagen biosynthesis in the ER?
A
1) Translation on the ribosome
2) Hydroxylation of Proline and Lysine.
22
Q
What are the next four steps of collagen biosynthesis inside the cell?
A
1) Release from ribosomes
2) Glycosylation
3) Triple helix formation (requires Vitamin C)
4) Secretion from the cell.
23
Q
What happens in steps 7-8 of collagen biosynthesis in the ECM?
A
1) Removal of N- and C-terminal domains
2) Crosslink formation.
24
Q
What happens to defective collagen chains that fail to form a stable triple helix?
A
They are immediately degraded within the cell, leading to blood vessel fragility and loss of tooth attachment.
25
What are the three phases of collagen homeostasis?
1) Synthesis (fiber and matrix maturation)
2) Degradation (natural breakdown by age, UV, and MMPs)
3) Stimulation (collagen fragments trigger new collagen production).
26
What are the four phases of bone remodeling?
Resting, resorption, reversal, formation.
27
What signaling molecule stimulates osteoclast differentiation and bone resorption?
RANKL (Receptor Activator of Nuclear Factor Kappa-B Ligand).
28
What molecule inhibits RANKL to prevent excessive bone resorption?
Osteoprotegerin (OPG).
29
How does chronic inflammation in periodontal disease affect bone remodeling?
Increases RANKL activation, leading to prolonged osteoclast activity and bone loss.
30
Which pro-inflammatory cytokines contribute to periodontal bone loss?
IL-1, TNF-α, IL-6.
31
What is the dental pellicle, and how does it form?
A proteinaceous layer derived from saliva, gingival crevicular fluid (GCF), and bacterial components; forms within minutes on clean enamel.
32
What is the function of the dental pellicle?
Provides protection, lubrication, and a surface for bacterial adhesion.
33
Which bacteria are primary colonizers in biofilm formation?
Gram-positive facultative aerobes like Streptococcus mitis, S. sanguinis, S. oralis, and Actinomyces species.
34
What is the role of Fusobacterium nucleatum in biofilm development?
Acts as a bridging species, connecting early and late colonizers.
35
Which bacterial species are part of the red complex, associated with periodontitis?
Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola.
36
What is the primary difference between primary and secondary colonizers?
Primary colonizers attach directly to the tooth surface, while secondary colonizers adhere to pre-existing bacteria.
37
What does the Non-Specific Plaque Hypothesis propose?
Disease results from overall plaque accumulation, regardless of bacterial species.
38
What is the main limitation of the Non-Specific Plaque Hypothesis?
Some individuals have heavy plaque but no disease, suggesting host factors play a role.
39
What does the Specific Plaque Hypothesis suggest?
Only certain bacterial species cause periodontal disease.
40
What is the main flaw in the Specific Plaque Hypothesis?
Periodontal pathogens can also be found in healthy individuals.
41
How does the Ecological Plaque Hypothesis explain periodontal disease?
A dysbiotic shift in the microbiome, driven by environmental changes, leads to disease.
42
What is the therapeutic goal of the Ecological Plaque Hypothesis?
Restore microbial homeostasis rather than eliminate all bacteria.
43
Which microbes are dominant in periodontal health?
Streptococcus mitis, S. sanguinis, S. oralis, Actinomyces viscosus, A. naeslundii.
44
How does the microbial composition shift in gingivitis?
Increase in Gram-negative anaerobes such as Fusobacterium nucleatum, Capnocytophaga, Prevotella intermedia.
45
What are the primary bacterial species associated with chronic periodontitis?
Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola.
46
What is the key pathogen in aggressive periodontitis?
Aggregatibacter actinomycetemcomitans.
47
What bacterial virulence factor allows P. gingivalis to adhere to host tissues?
Fimbriae that bind to fibrinogen and fibronectin.
48
How do endotoxins (LPS) contribute to periodontal disease?
They stimulate inflammatory cytokines (IL-1, TNF-α, prostaglandins) leading to bone resorption.
49
What bacterial enzyme degrades collagen in periodontal tissues?
Matrix metalloproteinases (MMPs).
50
How does biofilm contribute to gingivitis?
Plaque accumulation triggers an inflammatory response but does not cause attachment loss.
51
Which bacteria are commonly associated with gingivitis?
Streptococcus spp., Actinomyces spp., Fusobacterium nucleatum, Capnocytophaga, Prevotella intermedia.
52
How does biofilm contribute to periodontitis?
Biofilm leads to inflammation, tissue invasion, and alveolar bone loss when combined with a susceptible host response.
53
What microbial shift occurs in periodontitis?
From Gram-positive facultative bacteria to Gram-negative anaerobic species.
54
Name three bacterial species that invade periodontal tissues.
Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola.
55
What are the two primary goals of periodontal therapy regarding microbiology?
Reduce biofilm mass and create shallow gingival crevices to limit anaerobic bacterial growth.
56
What periodontal therapy methods reduce biofilm mass?
Scaling and root planing, antimicrobial agents, and improved oral hygiene.
57
How does reducing pocket depth help periodontal health?
Creates an environment less suitable for anaerobic Gram-negative bacteria.
58
What are two treatments used to reduce pocket depth?
Surgical intervention and host modulation therapy.
59
What are the clinical features of gingivitis?
Red, swollen gums, glossy appearance, no stippling, bleeding on probing, possible tenderness.
60
What histological changes occur in gingivitis?
PMN infiltration, increased GCF, vascular dilation, loss of 5-15% perivascular collagen.
61
What are the radiographic findings in gingivitis?
No bone loss, intact lamina dura.
62
What are the clinical features of periodontitis?
Red/bluish-red, swollen gingiva, gingival recession, pocket formation, tooth mobility, possible suppuration.
63
What histological changes occur in periodontitis?
Plasma cells/macrophages infiltrate connective tissue, apical migration of junctional epithelium, PDL and alveolar bone destruction.
64
What are the radiographic findings in periodontitis?
Horizontal/vertical bone loss, loss of lamina dura, widened PDL space.
65
What are the four lesions in the Experimental Gingivitis Model?
Initial lesion, early lesion, established lesion, advanced lesion.
66
What histological changes occur in the initial lesion (2-4 days)?
PMN infiltration, increased vascular permeability, slight collagen degradation.
67
What are the clinical signs of the initial lesion?
Subclinical, no visible changes, increased GCF.
68
What histological changes occur in the early lesion (4-7 days)?
T-cell infiltration, vascular proliferation, rete peg formation, 60-70% collagen loss.
69
What are the clinical signs of the early lesion?
Erythema, mild swelling, early gingival bleeding.
70
What histological changes occur in the established lesion (14-21 days)?
Plasma cell infiltration, increased pocket epithelium proliferation, further collagen degradation, no bone loss.
71
What are the clinical signs of the established lesion?
Chronic gingivitis, gingival enlargement, deeper pockets, continued bleeding on probing.
72
What histological changes occur in the advanced lesion?
Plasma cells/macrophages dominate, alveolar bone resorption, periodontal pocket formation.
73
What are the clinical signs of the advanced lesion?
Attachment loss, deep periodontal pockets, tooth mobility.
74
What is a gingival pocket (pseudopocket)?
A pocket formed by gingival enlargement without apical migration of the junctional epithelium.
75
What are the two types of periodontal pockets?
Suprabony and infrabony pockets.
76
What is a suprabony pocket?
A periodontal pocket where the base is coronal to the alveolar bone crest with horizontal bone loss.
77
What is an infrabony pocket?
A periodontal pocket where the base is apical to the alveolar bone crest with vertical bone loss.
78
What are the four zones of the root surface in periodontal pockets?
Cementum covered by calculus, attached plaque, unattached plaque, semi-destroyed connective tissue fibers.
79
How do bacterial endotoxins affect the root surface?
They penetrate the cementum, causing necrosis and demineralization.
80
What changes occur in the gingival wall of a periodontal pocket?
Accumulation of bacteria, leukocytes, inflammatory mediators, epithelial desquamation, ulceration, and hemorrhage.
81
What are the two main pathways of inflammation in periodontal disease?
Interproximal and facial/lingual pathways.
82
Describe the interproximal pathway of inflammation.
Gingiva → Periosteum, Periosteum → Alveolar bone, Gingiva → PDL.
83
Describe the facial/lingual pathway of inflammation.
Similar to the interproximal pathway, following blood vessels and collagen fiber bundles to the crestal bone.
84
What does the Episodic Burst Model propose?
Periodontal destruction occurs in bursts of activity and quiescence, rather than a continuous process.
85
What happens during periods of quiescence (inactivity)?
Reduced inflammation, little/no bone loss, decreased inflammatory mediators.
86
What happens during periods of exacerbation (activity)?
Increased Gram-negative bacteria, elevated cytokines (IL-1, IL-6, TNF-α), higher MMP activity, significant attachment loss, and bone resorption.
87
What is the definition of a risk factor?
Any environmental, behavioral, or biological factor associated with disease onset.
88
What are the two main categories of risk factors for periodontal disease?
Systemic risk factors and local risk factors.
89
How does age affect periodontal disease risk?
Older individuals experience more severe attachment loss.
90
Why do males have a higher prevalence of periodontal disease?
Due to differences in hygiene habits, hormones, or behavior.
91
How does socioeconomic status influence periodontal disease?
Lower status reduces access to dental care and education.
92
How do genetics and race contribute to periodontal disease?
Some individuals have genetic predispositions that affect immune responses.
93
How does smoking impact periodontal disease?
Increases bacterial colonization and decreases immune function.
94
Name three medical conditions that increase periodontal disease risk.
Diabetes, AIDS, osteoporosis.
95
How does stress affect periodontal health?
It impairs immune function and increases inflammation.
96
What are plaque-retentive factors that contribute to periodontal disease?
Calculus, caries, poor restorations, open contacts.
97
How can tooth morphology contribute to periodontal disease?
Furcations, root grooves, and enamel pearls make cleaning difficult.
98
What role does occlusion and trauma play in periodontal disease?
They can accelerate disease progression but do not initiate it.
99
What are endo-perio lesions?
Infections originating from the pulp that lead to periodontal destruction.
100
How do systemic risks contribute to periodontal disease?
They lower immune defenses, making tissues more vulnerable to infection.
101
How do local risk factors contribute to periodontal disease?
They promote bacterial colonization and inflammation.
102
What happens when risk factors persist over time?
The severity of periodontal disease increases.
103
What is the primary cause of periodontal disease?
A specific bacterial infection in biofilm.
104
How does plaque accumulation contribute to periodontal disease?
It triggers an inflammatory response that leads to tissue destruction.
105
What is essential for preventing periodontal disease?
Identifying and modifying risk factors.
106
What is the primary etiology of periodontitis?
Periodontitis is an inflammatory disease initiated by bacterial plaque.
107
Name three key periodontal pathogens.
Porphyromonas gingivalis, Tannerella forsythia, Aggregatibacter actinomycetemcomitans.
108
What are the virulence factors of periodontal bacteria?
Promote inflammation, evade the immune system, and contribute to tissue destruction.
109
Why does tissue damage occur in periodontitis?
Largely due to an exaggerated immune response rather than direct bacterial invasion.
110
What was the early model of periodontal disease pathogenesis?
It was thought that direct bacterial infection caused the disease.
111
How did the model shift in the 1980s?
Emphasis moved to the immune and inflammatory responses to plaque.
112
What is the current model of periodontal disease?
Periodontitis results from a dysregulated host response. Genetic and environmental factors influence disease progression. Inflammation can be both protective and destructive.
113
How does homeostasis disruption lead to periodontal disease?
Bacteria trigger chronic inflammation, leading to tissue breakdown.
114
Which inflammatory mediators contribute to tissue destruction?
IL-1, IL-6, TNF-α, PGE2.
115
How does tissue destruction occur in periodontitis?
MMPs (Matrix Metalloproteinases) degrade collagen, weakening tissues. Osteoclast activation leads to alveolar bone resorption.
116
What factors increase the severity of periodontal disease?
Genetic susceptibility, smoking, diabetes, and environmental factors.
117
What are the key cells of innate immunity in periodontal disease?
PMNs (Neutrophils): First line of defense, phagocytose bacteria. Macrophages: Release pro-inflammatory cytokines in response to LPS. Toll-Like Receptors (TLRs): Recognize bacteria, activating NF-kB and inflammation.
118
What are the key adaptive immune cells in periodontal disease?
Th1 Cells: Promote inflammation. Th2 Cells: Enhance antibody production. Th17 Cells: Secrete IL-17, stimulating osteoclast-mediated bone resorption. B Cells: Produce antibodies but also contribute to inflammation.
119
Name key pro-inflammatory cytokines in periodontitis.
IL-1, IL-6, TNF-α, PGE2.
120
Name key anti-inflammatory cytokines in periodontitis.
IL-10, IL-4.
121
What enzymes are responsible for collagen degradation?
Matrix Metalloproteinases (MMPs).
122
What happens when MMPs are overexpressed?
Excessive breakdown of connective tissue.
123
What is the RANK/RANKL/OPG pathway?
RANKL: Stimulates osteoclasts → bone resorption. RANK: Receptor on osteoclast precursors; activation leads to bone loss. OPG: Inhibits RANKL, preventing excessive bone resorption.
124
How does inflammation drive bone resorption?
Bacterial LPS and inflammatory cytokines increase RANKL, leading to increased osteoclast activity and alveolar bone loss.
125
What is the primary role of PMNs in periodontal disease?
They act as the first line of defense, clearing bacteria through chemotaxis, phagocytosis, and antimicrobial enzyme release.
126
What happens in PMN dysfunction due to Leukocyte Adhesion Deficiency (LAD-1)?
Defective PMN recruitment leads to persistent bacterial infection, increased IL-17, and bone resorption.
127
How does PMN hyperactivity contribute to periodontal destruction?
Excessive release of hydrolytic enzymes and reactive oxygen species damages tissues.
128
What happens when PMNs are hypoactive?
Reduced bacterial clearance leads to immune dysregulation and increased periodontal destruction.
129
How do Th1 cells contribute to periodontal disease?
They secrete IFN-γ, enhancing macrophage activation and inflammation.
130
What is the role of Th17 cells in periodontitis?
They produce IL-17, promoting osteoclastogenesis, bone resorption, and excessive inflammation.
131
How do B cells contribute to periodontal destruction?
They produce antibodies against periodontal pathogens and increase RANKL, leading to bone loss.
132
Which cytokines drive periodontal tissue destruction?
IL-1, IL-6, TNF-α, PGE2.
133
How does an increased RANKL/OPG ratio affect alveolar bone?
It leads to enhanced osteoclast activity and bone loss.
134
What are pro-resolving lipid mediators, and what do they do?
Lipoxins, resolvins, and protectins derived from polyunsaturated fatty acids that reduce PMN infiltration and resolve inflammation.
135
How does RvE1 treatment help in periodontitis?
It prevents bone loss, reduces inflammatory cytokines, and improves bacterial balance.
136
Name three types of host-modulation therapy used in periodontal treatment.
COX Inhibitors (NSAIDs): Reduce prostaglandin-mediated inflammation.
Denosumab: Blocks osteoclast activity, reducing bone loss.
Anti-cytokine Therapy: Targets IL-1, IL-17, and TNF-α to control inflammation.
137
What is the modern multifactorial model of periodontitis?
It results from microbial dysbiosis, host immune response, and genetic/environmental risk factors.
138
How is periodontitis linked to systemic diseases?
Periodontopathic bacteria can enter the bloodstream, triggering systemic inflammation, contributing to diseases like diabetes and cardiovascular conditions.
139
What role do excessive cytokines play in periodontitis?
Overexpression of IL-1, IL-6, TNF-α, PGE2, and MMPs leads to periodontal tissue breakdown.
140
What are the future research directions in periodontal disease?
Precision medicine: Targeting immune dysregulation.
Biomarkers: Predicting disease progression and treatment response.
141
What scientific evidence links genetics to periodontal disease?
Twin and family studies show genetic heritability influences disease susceptibility.
142
What periodontal condition is strongly linked to genetic predisposition?
Stage 4, Grade C periodontitis (formerly aggressive periodontitis).
143
What genetic defects are associated with aggressive periodontitis?
Neutrophil function defects and single nucleotide polymorphisms (SNPs) in immune response genes (e.g., IL-1, TLR-4).
144
Which racial group has a higher prevalence of early-onset periodontitis?
African Americans.
145
What is a Single Nucleotide Polymorphism (SNP)?
A single base-pair change in DNA that affects protein function and immune response.
146
What is an Insertion/Deletion Polymorphism?
The addition or removal of DNA segments that influence gene expression.
147
What is a Microsatellite Polymorphism?
Repetitive DNA sequences that vary in length, affecting gene regulation.
148
What is a Copy Number Variant (CNV)?
Variations in the number of copies of a gene, influencing disease susceptibility.
149
What is the role of IL-1 in periodontal disease?
IL-1 is a pro-inflammatory cytokine that promotes immune response and bone resorption.
150
How do IL-1 gene polymorphisms affect periodontal disease risk?
Variants in IL-1α and IL-1β (on chromosome 2) lead to higher IL-1 production, increasing inflammation and rapid periodontal breakdown.
151
What clinical signs are associated with IL-1 polymorphisms?
Increased inflammation, more bleeding on probing (BoP), and faster periodontal destruction.
152
What is epigenetics?
Modifications in gene expression without changing the DNA sequence.
153
What are two major epigenetic mechanisms affecting periodontitis?
DNA methylation and histone modifications.
154
How does epigenetic therapy help manage periodontitis?
It reverses harmful gene expression changes, such as excessive inflammatory cytokine production.
155
What is Apabetalone (RVX-208), and how does it work?
A drug that interferes with gene transcription, reducing inflammatory gene expression and preventing osteoclast differentiation and bone loss.
