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Oral Soft Tissues Exam I Review Flashcards

1
Q

Regarding the Pathogenesis Human Periodontitis Model, what are the risk factors for the Host Immuno-Inflammatory response and CT & bone metabolism?

A

1) Environmental Factors

2) Genetic Risk Factors

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2
Q

Regarding the Pathogenesis Human Periodontitis Model, Clinical Signs of disease initiation and progression lead to what?

A

Microbial challenge

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3
Q

Regarding the Pathogenesis Human Periodontitis Model., What 2 factors leave the “Host Immuno-inflammatory response to the CT & bone metabolism?

A

1) Cytokines & Prostanoids

2) MMP (Matrix metalloproteinases

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4
Q

The Microbial Challenge will present ______________ and ______________ to the Host ImmunoInflammatory response?

A

1) Antigens

2) Lipopolysaccharide
& Other virulence factors

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5
Q

The Host Immuno Inflammatory Response will present ______________ and ______________ to CT & bone metabolism?

A

1) Cytokines & prostanoids

2) Matrix metalloproteinases

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6
Q

CT & bone metabolism will lead to what——-> _______

A

Clinical signs of signs of disease initiation & progression

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7
Q

2) What causes periodontal disease cause?

A
  • *Bacterial plaque- are essential but insufficient to cause disease
  • *Susceptible host- such as heredity, and environmental factors such as smoking are equally as important as bacteria in determining disease occurrence and severity of disease outcome.

• Microbial Risk Factors:
o Specific microorganism
o Total microbial burden
o Biofilm pathogenicity

•	Systemic Risk Factors:
o	Diabetes
o	Genetic Factors
o	Sex/Race
o	HIV
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8
Q

3) What is the most common form of periodontal disease?

A

Majority have Slight (mild) PD

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9
Q

4) What is important in diagnosing periodontal disease?

A
  • Color
  • Countour (form)
  • Consistency (density)
  • Probing Depths
  • Clinical Attachment Loss **
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10
Q

5) What are the tissues of the periodontium and of the attachment apparatus?

A

1) Gingiva and alveolar mucosa

2) Periodontal attachment apparatus
- PDL
- Cementum
- Alveolar Bone

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11
Q

6) What is the MGJ? (Mucogingival Junction)?

A
  • MGJ does not change , that line is permanent
  • Location: base of gingival mucosa & top of alveolar mucosa
  • MGJ is pt at which keratinized & non-keratinized epithelium meets
  • Keratinized epithelium goes to gingival epithelium → MGJ
  • Attached gingiva is measured from gingival sulcus (GM) to MGJ minus PD
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12
Q

7) Know the difference between keratinized & mucosal tissue?

A

• Keratinized Gingiva and Mucosal Epithelium separated by Mucogingival junction (MGJ)

Keratinized*
• Oral/Outer Epithelium: Keratinized or parakeratinized (0.2-0.3mm)
- HARD PALATE (MOST keratinized), Cheek (LEAST keratinized)
- Turnover 10-12 days

•	Keratinized & Attached Gingiva:
-	KG = GM to MGJ
-	AG = GM to MGJ minus PD
-	AG = KG minus PD 
•	Keratinization of mandible
•	MOST = Incisors 
•	LEAST  = Premolar

• Gingival width:
Incisors > Molars > Premolars

  • Alveolar Mucosal**
  • Non-keratinized epithelium
  • Smooth, shiny surface
  • Reddish
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13
Q

8) Where do you commonly find the most and least attached tissue?

A

1) Crevicular epithelium (aka free gingiva) is the least attached tissue.
2) Junctional epithelium is the most attached gingiva.

  • Two mathematical equations to determine the attached gingiva
    1. AG= KG - Probing Depth
    1. AG= (GM to MGJ) - Probing Depth
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14
Q

9) Know the 3 different types of epithelium (***oral, sulcular, junctional)

A
  • Oral or outer epithelium
  • Keratinized or parakeratinized
  • 0.2-1.3 mm thick
  • Keratinization
  • Palate = Most
  • Cheek = Least
  • Keratinocytes
  • Nonkeratinocytes
  • Melanocytes
  • Langerhan’s cells
  • Merkel cells
  • Turnover 10-12 days
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15
Q

9) Know the 3 different types of epithelium (oral, ***sulcular, junctional)

A
  • Crevicular (Sulcular) Epithelium
  • Similar to oral Epithelium
  • Resistant to fluid flow
  • Nonkeratinized, thin and without rete pegs
  • Has the potential to keratinize
  • Extends from GM to JE
  • Has potential to keratinize
  • Extends from GM to coronal limit of JE
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16
Q

9) Know the 3 different types of epithelium (oral, sulcular, **junctional)

A
  • Junctional Epithelium
  • Non-keratinized
  • 2-30 cells thick
  • 0.25-1.35 mm length
  • Hemidesmosomes
  • Cell to tooth/implant
  • Cell to connective tissue
  • *Same for tooth/implant
  • Turnover 1-6 days
  • Attachment
  • Internal Basal Lamina
  • To tooth or implant
  • Lamina densa
  • Lamina lucida
  • External basal lamina
  • To connective tissue
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17
Q

10) Know about junctional epi (Attached) and what it is?

A
  • Non-keratinized
  • 2-30 cells thick
  • 0.25-1.35 mm length
  • Hemidesmosomes
  • Cell to tooth/implant
  • Cell to connective tissue
  • *Same for tooth/implant
  • Turnover 1-6 days
  • Attachment
  • Internal Basal Lamina
  • To tooth or implant
  • Lamina densa
  • Lamina lucida
  • External basal lamina
  • To connective tissue
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18
Q

11) What is stippling, turn over of cells, etc.

A

1) Oral or outer epithelium
- Keratinized or parakeratinized
- Turnover 10-12 days

2) Crevicular (Sulcular) Epithelium
- Non-keratinized (has potential to keratinize), thin and without rete pegs

3) Stippling
- Depressions/ raised areas in surface of attached gingiva
- Occurs at sites of rete pegs

4) Junctional Epithelium
- Non-keratinized
- Turnover 1-6 days

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19
Q

12) PDL what are the terminal fibers called?
- What are cell types?
- What’s it made up of?
- Function?
- Where is it not found?
- What is the width?

A
  • PDL is a group of principal fibers that insert into cementum & alveolar bone.
  • Sharpey’s fibers are the terminal portion of the principal fibers.
  • PDL is composed of CT cells (Fibroblasts, Cementoblasts & Osteoblasts), Host Defense Cells & Rests of Malaise (isolated clusters of epithelium)
  • PDL functions to transmit forces & maintain attachment.
  • PDL has a width of 0.1-0.2mm.
  • PDL is not found in implants (implants form hemidesmosomes w/ alveolar bone)
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20
Q

13) What are the gingival fibers group made up and their functions?

A

Gingival Fibers:

1) Circular: support & contour to free gingiva
2) Gingivodental group:
- Dentogingival: support of gingiva
- Dentoperiosteal: anchors tooth to bone
- Alveologingival: attaches gingiva to alveolar bone

3) Transseptal fibers: keep teeth in alignment and protects bone; continuously reform as bone and fibers are destroyed
- *Not on implants: dentogingival, dentoperiosteal, transseptal

21
Q

13) What make up and periodontal group and their functions

A

Periodontal fibers:
1) Alveolar crest: resists lateral movement

2) Horizontal: opposes lateral forces
3) Oblique: absorbs occlusal forces: largest group
4) Apical: resists tipping of tooth
5) Interradicular: resists forces of lunation (pulling out) and tipping

22
Q

14) What is biological width and the number & what it is made up of?

A

***BIOLOGICAL WIDTH: (aka Gingival Attachment, Physiologic Dentogingival Junction)

1) Physiologic zone of gingival tissue coronal to the alveolar bone crest
2) Composed of the epithelial attachment and the gingival connective tissue attachment

  • Junctional Epi:
    0. 97 mm “C”
  • Connective Tissue:
    1. 07 mm “D”
  • Biologic Width:
    2. 04 mm “A”
  • *Violations of the biologic width:
    1) Inflammation
    2) Increasing probing depth
    3) Inconsistent resorption of alveolar bone
23
Q

15) Be able to calculate Clinical Attachment Loss via numbers or words, what is it?

A

a. Distance from the CEJ to the base of the crevice.**
b. Calculated – not measured
c. CAL = PD (mm) + CEJ to GM (mm)
d. CEJ to GM may be:
i. (+) Positive if apical to CEJ (i.e recession present)
ii. (-) Negative if coronal to CEJ (i.e excess tissue covering)
f. Tissue apical to CEJ: we take that Number add it to pocket number = attachment loss
g. Coronal to CEJ = Excess tissue. Subtract it from pocket number

***Probing Depth Measurement + Gingival Margin Level ( + if Apical to CEJ or - if Coronal to CEJ) = CAL

24
Q

16) Know types of gingivitis plaque induced ?

A

Plaque induced:

  • Systemic factors
  • Endocrine (puberty, pregnancy, diabetes)
  • Blood dyscrasias (leukemia)
  • Drugs: tx via cauterizing the tissue/vessels (dec bleeding), will come back as long as pt is on the medication
  • Anti-seizure meds (Dilantin)
  • Ca channel blockers (Nifedipine)
  • Immunosuppressants, ex: with transplant pts (Cyclosporin)
  • Oral contraceptives
  • Malnutrition → rare in US
  • Vit deficiency
  • Scorbutic gingivitis “Scurvy”
25
16) Know types of gingivitis non-plaque induced(***viral) ?
Non-plaque induced: 1) Bacteria: E. Coli, Streptococcus, Neisseria, Treponema 2) VIRUSES: Herpes 3) Fungal infections: Candidiasis, Histoplasmosis 4) Systemic diseases: Benign Mucous Membrane Pemphigoid, anywhere there is a mucous membrane 5) Trauma: toothbrush abrasion 6) Foreign Body reactions: popcorn kernel, dental materials, ortho brackets 7) Genetic: Hereditary Gingival Fibromatosis
26
17) What type of category does pregnancy and gingivitis fall into
- Pregnancy associated gingivitis: Plaque-induced gingivitis - Inc [prevotella intermedia] → uses steroids as growth factor - Will go away once done w/ pregnancy - Tx: cleaning and debridement, OH (prophy, cavitron), antibacterial mouthwash (chlorhexidine)
27
18) Know medications involved in gingival growth
(“Plaque-Induced Gingivitis, Modified by Medication”) 1) Anti-Convulsants/Anti-Seizure - Dilantin* 2) Calcium Channel Blockers - Nifedipine* 3) Immunosuppresants - Cyclosporin * 4) Oral Contraceptives * "Gingival enlargements"
28
19) Epidemiology slides: risk and risk factors what do those mean
- RISK - The likelihood a person will get a disease in a specified time period - RISK FACTOR - Before manifestation, a factor that puts them at a greater risk for developing the disease
29
20) Microorganisms in periodontal disease?
1) Chronic PD: (pg, tf, td, aa) - Porphyromonas gingivalis (Proteases) - Tannerella forsythia - Treponema denticola - Aggregatibacter actinomycetemcomitans (leukotoxin) 2) Aggressive PD: (aa, pg) - Aggregatibacter actinomycetemcomitans (leukotoxin) - Porphyromonas gingival is (some patients) (proteases) 3) Necrotizing PD: (Pi) - Prevotella intermedia (also seen in pregnancy-associated gingivitis) - Spirochetes (invade CT) - Fusiform bacilli
30
21) Know what a biofilm is ? Why is it important in dentistry
* Dental plaque is a biofilm -> cooperating community of microorganisms arranged in micro colonies surrounded by protective matrix * Different environments within micro colonies * Microorganisms have primitive communication system * Bacterial pathogenicity and virulence expression may be enhanced * Resistant to antibiotics, antimicrobials and the host response (antibodies/PMNs) * Plaque spreads apically along root surface
31
22) Know about plaque? (tooth associated, tissue associated, gram +, cocci, how does it shift from healthy to disease what do we start to see) * TOOTH Associated Subgingival Plaque?
TOOTH Associated Subgingival Plaque - Densely, adherent, biofilm - G+ rods, cocci, filaments - Facultative aerobes/anaerobes - Remove by SRP (mechanical removal) - Less virulent
32
22) Know about plaque? (tooth associated, tissue associated, gram +, cocci, how does it shift from healthy to disease what do we start to see) * TISSUE Associated Subgingival Plaque:?
TISSUE Associated Subgingival Plaque: - Loosely adherent - G- motile anaerobes - Spirochetes - Remove surgically - More virulent
33
22) Know about plaque? (tooth associated, tissue associated, gram +, cocci, how does it shift from healthy to disease what do we start to see) ***Unattached Subgingival Plaque
Unattached Subgingival Plaque - “Free swimming” in pocket - G- motile anaerobes - Spirochetes - Remove by flushing - More virulent
34
22) Know about plaque? (tooth associated, tissue associated, gram +, cocci, how does it shift from healthy to disease what do we start to see) **Microbial Shift:
Microbial Shift: Healthy -> Gingivitis -> Periodontitis - From G+ to G- - From Cocci to rods (later spirochetes) - From non-motile to motile - From facultative to obligate anaerobes
35
23) Know about calculus and its role?
1) Calcified dental plaque 2) Roughness increases surface area 3) NOT a mechanical irritant 4) Increases density in which plaque can accumulate 5) Increases bacteria concentration 6) SECONDARY contributing factor to PD 7) Color: - Supragingival: whitish yellow - Subgingival: dark brown, hard & dense 8) HARBORS BACTERIA → Induces DAMAGE
36
24) Know what cells first come into pocket (3). What do they do?
1) PMN: 1st responder, migrates into sulcus/pocket - phagocytize 2 )Mast Cell: releases amines - increases vascular permeability 3) Macrophage: present antigen to T-cells 4) T-lymphocytes: lymphokines and delayed hypersensitivity 5) B-lymphocytes: may differentiate into plasma cells - Active in antibody formation
37
25) Paige and Schroder graphs (initial, early lesions , clinical signs, how long before signs show up?)
***Pathogenesis Stages*** 1) INITIAL: Increased GCF (gingival crevicular fluid), tissue looks wet. Acute Inflamm: Vasculitis, PMNs, Mac's, (2-4 days) 2) EARLY: Start to see signs of gingivitis (redness/bleeding/edema), T-cell lesion (4-7 days) 3) ESTABLISHED: B-cell lesion, plasma cells, Chronic Gingivitis (2-3 wks) 4) ADVANCED = periodontitis (B-cell lesion, bone loss, pocket formation) ( Unknown time or if gingivitis will ever develop into periodontitis)
38
26) Know the difference between ***cytokines IL, TNF, what causes bone destruction?
IL-1β (Interleukin-1) - CYTOKINE - Bone resorption - Genetic Influences: Interluekin-1 slide - Polymorphisms in the gene cluster associated with the activity of IL-1 are responsible for a 2-4 times increase in macrophage IL-1 production. - Individuals with this IL-1 profile have more severe periodontal disease. - The polymorphism does not cause the disease, it makes the individual response more severe
39
26) Know the difference between cytokines IL, ****TNF, what causes bone destruction?
TNFά - CYTOKINE - Bone resorption (with PGE2)
40
26) Know the difference between cytokines IL, TNF, & MMP's. What ***causes bone destruction?
MMP(1&8) - PROTEINASES (NOT A CYTOKINE but found with them) - Connective tissue breakdown - Collagenases - Elastase - Degradation of extracellular matrix molecules - “Breakdown Collagen”
41
27) Know the advanced lesions (IRREVERSIBLE) advanced lesion of paige & Schroder
- Alveolar bone loss - Pocket formation - Periodontitis = advanced lesion - B-cell lesion (name of cells involved) - Irreversible - Undetermined amount of time of onset
42
28) Know about SMOKING, effects on TX, problems in smoking, What do we see in immune response?
- DEC. clinical expression of inflammation, LESS clinical inflammation - Causes LOCALIZED Attachment LOSS & “leathery” gingiva - SMOKELESS Tobacco: Leukoplakia carcinoma, NO effect on periodontitis - Smoking effects are reversible w/ cessation - Current smokers = 4x risk of peril disease, former smokers = 1.6x risk - Smoking has NO EFFECT on RATE of Plaque Accumulation - INCREASE pathogens in shallow & deep pockets - Causes DECREASED immune response, PMN, chemotaxis, phagocytosis - Causes INCREASE TNF-alpha, PEG2 & MMP-8 - Smokers have DECREASE response to Tx: LESS reduction of pocket depths, LESS regenerative response, INCREASE likelihood of failed implants, DECREASE response to scaling & root planing, LESS pocket depth reduction, LESS gain in attachment, INCREASE in pocket depth, DECREASE in attachment gain - GREATER risk of recurrence (relapse) & refractory (non-responsive to tx modalities) - Overall MORE tooth loss - Smokers are good candidates for PerioStat drug therapy (antibiotics)
43
29) Host Modulatory response? What does it do and how does it do it? What is the goal?
- Normal host response does a significant portion of the damage seen in periodontal disease. Host response is mediated by : 1) MMPs such as collagenase - Produce collagen breakdown 2) Prostaglandins - Produce bone resorption 3) Osteoclasts - Produce bone resorption * Host modulation is regulating the tissue damaging host response, typically using drugs. - Target MMPs, Prostaglandins, Osteoclasts * Major drug for host modulation - Periostat, which is a small dose of the antibiotic doxycycline - Inhibits MMP at 20 mg 2x a day and didn’t alter immune susceptibility (100mg tablets, cut into 4, 1 in AM and 1 in PM) → put collagenase pharmaceuticals out of business
44
30) When you collect data what is most important when you collect it when diagnose perio disease?
- CAL: Clinical Attachment Loss - Probing Depth Measurement + Gingival Margin Level (+ or - ) = CAL - If we saw the patient today & took data, and we saw them months later & took data how can we tell there was a continuation of the disease CAL & probing depths increasing can tell you if disease is getting worse!
45
31) Know what healthy gingiva and what disease gingiva looks like?
Healthy: - Scalloped gingival margin - Papillas between the teeth are knife-like - Pink (salmon) indicative of health Diseased (1-5) - Blunted/bulbous/rounded interproximally - Engorged - Vasculature - Red is diseased (inflammation) - Increased bleeding on probing - Loss of clinical attachment levels/recession - Loss of soft and hard tissues - “Only increasing probing depths and clinical attachment loss are associated with disease progression” - If smoker - tissue will be fibrotic and not show lots of bleeding (1-7)
46
32) Know cementum (bc it is apart of attachment apparatus)
* Calcified substance that covers root. - Can have Overlap (60-65%), Butt (30%) or Exposed Dentin (5-10%) at the cementoenamel junction. Dimensions: - 16-60 microns coronal - 150+ microns apical - apical, furcal and distal surfaces increases with age - Cementum increases in width with age - Attaches teeth to alveolar bone by anchoring PDL (Sharpey's fibers inserts into cementum)
47
What makes up gingiva?
1) Marginal - Free - Gingival sulcus 2) Attached gingiva 3) Interdental gingiva
48
In a HOST MODULATION RESPONSE what will shift the scale to HEALTH?
1) Reduction of risk factors 2) Expression of host-derived anti-inflammatory or protective mediators (IL-4..etc) 3) Host modulatory therapy 4) Resolution of inflammation 5) OHI, SRP, Surgery, antiseptic, antibiotics, to reduce bacterial challenge
49
In a HOST MODULATION RESPONSE what will shift the scale to DISEASE?
1) Risk factors (genetics, smoking, diabetes) 2) Overproduction of proinflammtory or destructive mediators & enzymes (e.g IL-1, PGE2, TNF-a, MMPs) 3) Underactivity or overactivity of aspects of host response 4) Poor compliance Poor plaque control 5) Subgingival bioburden

Oral Soft Tissues (3 decks)

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