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Oral Boards Fall 2021 > Previous Oral Boards Questions/Topics #2 > Flashcards

Previous Oral Boards Questions/Topics #2 Flashcards

1
Q

What are some Virulence factors of p gingivalis

A
  • Gingipains: can induce MMPs with damage tissues
    • Invasion can occur via gingipain proteases
  • Fimbriae: P.g. does initial binding via adhesins: major fimbriae (FimA) and stimulate immune response
  • LPS: acts as endotoxin, found in the outer membrane of gram negative. Protect structural integrity of cell
  • Capsule: Major surface antigen
  • P.g can invade epithelial cells
  • Pg can facilitate invasion of T forsythia into epithelial cells
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2
Q

What is Inflammation?

A

The immune systems response to an irritant. So a foreign body or or irritant begins the inflammatory cascade, which begins with IL-6 and the innate immune system, recruiting PMNs. Then later we get into the adaptive immune system

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3
Q

Talk about Junctional Epithelium (JE) desmosome attachments and how many there are and why that’s important

A

Desmosome 2 dense attachment plaques (one from each cell) into which tonofilaments (cytoskeleton of keratin proteins) insert from each cell, forming an intermediate electron-dense line in the extracellular compartment

JE: attaches to tooth surface (via hemidesmosomes, laminin)

2 dense attachment plaques w tonofilmaments

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4
Q

What type of Collagen is the PDL

A
  • Type I collagen (80%)
  • Type III collagen (20%)
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5
Q

How good are we at prognosis?

A

Bad

McGuire classification

  • only good at determining “Good prognosis” We are not good at determining fair, poor, questionable and hopeless prognosis because it is very subjective.
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6
Q

What is the McGuire Prognosis Classification based on?

A

Survivability

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7
Q

What are the grade modifiers in the new classification system

A

Smoking >10 cigarettes

Diabetes HbA1c <7.0%

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8
Q

What are the Mechanisms of Diabetic Influence on the Periodontium?

A

1. Altered Microbial Composition

2. Increase GCF Glucose Concentration

3. Vascular Changes

4. Impaired Host Defenses

  • AGE Formation (affects fibroblast activity- enhanced host inflammatory response)

5. Impaired Collagen Metabolism

  • AGE Formation
  • Collagenase
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9
Q

Provide some evidence of how Diabetes increases the risk for Periodontal Disease

A

(Lalla)—perio ; type 1

  • kids with diabetes (type 1) had poorer periodontal parameters than controls; same microbial profiles- risk increased with age
  • 6-11 years old: O.R. = 3.44 for diabetes
  • 12-18 years old: O.R. = 20.3 for diabetes

(Tsai)—type 2; Poorly controlled DM subjects were 2.9 times more likely to have severe periodontitis than non-DM subject

(Emrich)—type 2; Pima Indians - DM2 has an OR of ~3.0 for periodontal disease in cross sectional study

(Polak)- Elevated levels of IL-1b, IL-6, and RANKL/OPG ratios have been demonstrated in periodontitis patients with DM.

  • PDL fibroblast activity is affected by high levels of AGE in gingival tissues (due to hyperglycemia), causing fibroblast secretion of inflammatory mediators
  • changes in their RANKL/OPG ratio which lead to increased bone resorption
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10
Q

How does Presence of Periodontal Disease increase risk for Diabetes

A

(Polak)

  • Untreated Periodontitis –>
    • Circulating bacteria/bacterial antigens
    • Elevated circulating levels of IL-6, TNF-a, CRP, Oxygen Radicals
  • Systemic Inflammatory State & Impair Insulin Signaling/Resistance
  • Exacerbation of Diabetes–>
  • Elevated HbA1c Levels –>
  • Increased Diabetes Complications

CHANGES THE WAY THE BODY USES INSULIN

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11
Q

What is the difference between Incidence and Prevalence?

A

Incidence = rate at which event occurs

  • Number of new cases that develop the disease in a given amount of time
  • How many people will develop covid over the next month

Prevalence = # of cases of disease in a population at a given time

  • Number of people with a disease at a given time
  • How many people have covid in Texas RIGHT NOW
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12
Q

Your patient is having an asthma attack: Asthma attack – How would you manage the patient & how much epinephrine would you give and would you increase the dose each time or not

A

Bronchospasm: reversible reflex spasm of smooth muscle in the bronchi

  • Wheezing, cough, dyspnea, increased anxiety
  • Allow patient to sit as they please, upright preferred
  • Administer Albuterol prn, 5 min onset (Beta-2 agonist inhaler: bronchodilator)
  • Re-administer as necessary
  • 100% Oxygen 10 L/min

Epinephrine 0.3mg IM if not responsive to Albuterol

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13
Q

Is there such thing as Titanium allergy?

A

Reports of type IV hypersensitivity reactions to titanium

Symptoms: urticaria, eczema, and mucosal erythema.

  • Some reports show de-keratinized hyperplastic reactions of the peri-implant tissue and drug rash with eosinophilia and systemic symptoms, associated with titanium implants.
  • Reports have shown that problems such as muscle and joint pain and chronic fatigue syndrome have appeared after titanium materials (implants, braces, endoprostheses) were put in patients.

Prevalence of titanium allergy is 0.6%. (Sicilia et al)

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14
Q

Pathogenic mechanisms Diabetes & Periodontal disease (Talk about a few of them)

A
  • Few differences in microflora of diabetes patient
  • GCF: inc glucose levels (alter wound healing)
  • AGEs: collagen accumulation at BM, inc thickness of BV walls
    • causes altered response to pathogens
  • Altered host defense: PMN adherence, chemotaxis, phagocytosis impaired
    • allows inc proliferation of pathogenic organisms
    • monocytes: hyperresponsive with diabetes
    • inc production of cytokines
    • in response to p. gingivalis: 32x more TNF-A (Salvi)
    • inc IL-1B, PGE2
  • Changes in collagen metabolism: alters turnover
    • MMP: collagenase inc with diabetes
    • Readily degrades newly formed collagen
    • Periodontium unable to repair itself
    • Accumulation of AGE modified older collagen
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15
Q

What are the Gingival Fiber Groups (8)

A
  1. Dentogingival
  2. Dentoperiosteal
  3. Alveologingival
  4. Circumferential
  5. Semi Circular
  6. Transgingival
  7. Intergingival
  8. Trans Septa
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16
Q

What are the functions of Gingival Connective Tissue (CT) making up the Gingival Fibers

What type of Gingival Fibers forms with Implants?

A
  • provide stability, esp with significant bone loss
  • can explain increased mobility following perio sx
    • due to disruption of gingival fibers
  • circular gingival fibers: responsible for gingival connection to implants
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17
Q

What is the Width of the PDL space

A

0.1 to 0.25mm

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18
Q

Explain the RANKL/OPG pathway and what systemic diseases are affected by this pathway

A
  • RANK receptor on osteoclast
  • produced by lymphocytes: RANKL
  • RANK-L/ OPG ratio = bone loss
  • Balance between OPG and RANKL activity can therefore drive bone resorption or bone formation

RANK ligand is the primary mediator of bone resorption. Osteoprotegerin (OPG) provides an alternative binding site for RANKL and acts as a decoy receptor by blocking RANK ligand binding to its cellular receptor RANK. Ligand binding activates cellular signalling. Ligand that is bound to a decoy receptor cannot activate cellular signalling

IL-IB and TNF-A have elevated levels of proinflammatory cytokines and increasing numbers of infiltration T cells results in the activation of osteoclasts via RANK

Systemic Diseases

  • Diabetes
  • Osteoporosis
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19
Q

List and describe the 4 types of Dental Calculus

A

1. Brushite

  • Dominant form in newly formed supragingival calculus and decreases as the calculus ages; yellowish-white crumbly deposit that is easily removed

2. Octacalcium phosphate

  • Increases as the calculus ages and is at higher amounts in subgingival calculus making it harder; predominates in superficial layer of calculus

3. Hydroxyapatite

  • Increases as the calculus ages and predominates subgingival calculus;

4. Magnesium whitlockite

  • Increases as the calculus ages
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20
Q

What are the two methods of Calculus Deposition

A

1. Epitactic - which says calculus forms by crystal seeding in plaque

  1. Booster - which says increases in local pH by urea and ammonium bi products causes precipitation of minerals
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21
Q

How does Calculus Attach to the Cementum

A
  1. Attachment to dental cuticle (organic pellicle on enamel)
  2. Attachment through micro irregularities in the surface left by Sharpey’s fibers
  3. By bacterial penetration into cementum (debunked)
  4. Attachment into cemental mechanical undercuts due to resorption areas

(Zander)

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22
Q

Describe the Stages of Gingival Inflammation

A

Page and Schroder

1. Initial lesion

  • PMN (neutrophils) dominate the lesion
  • Vasodilation occurs
  • Increased intracellular spacing
  • Small areas of collagen loss
  • Appears 2-4 days

2. Early Lesion

  • T-cells dominate the lesion (80%T, 20%B)
  • 10-15% loss of CT
  • 60-70% loss of perivascular collagen
  • Appears 4-7 days

3. Established Lesion

  • B-cells dominate the lesion
  • JE proliferate in apical direction
  • Further increase in CT breakdown
  • Basal cells begin to replicate apically into CT
  • Appears 2-3 weeks

4. Advanced Lesion

  • B-cell predominates still
  • Bone loss occurs
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23
Q

How accurate is the “furcation arrow” in detecting actual furcation invasions in maxillary molars

A

Deas furcation study

Sensitivity was only 39%, specificity was 92%, Pv(+) was 72%

  • If Clinically and truly present- found only 39% was it shown on X-ray
  • If on x-ray only 72% seen clinically
  • Low sensitivity (39%)—radiograph positive 39% of the time when furcation actually there, high specificity

WHAT YOU NEED TO KNOW is PPV = 72% (when you see a furcation arrow on an X-ray, there’s only a furcation invasion 72% of the time)

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24
Q

What are clinical signs of Gingivitis?

A
  • Inflammation
  • Bleeding on Probing
  • No Attachment Loss
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25
Q

Talk about smoking’s effect on periodontium and on implants survival ? when a smoker is the same as non smoker

A
  • Takes 11 years of no smoking to return to levels of a non-smoker (Tomar and Asma) (NHANES)
  • Systematic review for smoking and implant therapy, smoking is a risk factor for implant therapy (Heitz Mayfield)
  • Every year you quit smoking, your risk decrease by ~2.5% (Al harthi)
26
Q

CBCT– what artery runs through the sinus

A

Posterior superior alveolar artery

Infraorbital Artery (usually runs in conjunction with Posterior superior alveolar artery)

27
Q

What are Koch’s Postulates?

A
  1. Organism found in the lesion/disease but not in healthy organisms
  2. Must be isolated and grown in culture on artificial media
  3. The cultured microorganism should cause disease when introduced into a healthy organism
  4. The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent

Proof that bacteria can cause periodontal disease

(specific organisms can cause disease)

28
Q

Why are Kosch’s postulates wrong?

A
  • Can’t be satisfied because some pathogens can’t be grown on artificial surfaces, and some are only pathogenic for humans (species specific)
29
Q

What are the alternative criteria to Koch’s postulates?

A

Socransky’s postulates

1. Association with the disease: thus the pathogen must be at significantly higher levels in the diseased site as oppose to the healthy

2. Elimination of the organism: Elimination of the pathogen should arrest the disease

3. Host response: The host response to the pathogen should be greater as compared to non-pathogens

4. Animal Pathogenicity: Placing the pathogen in germfree animals or conventional animals should cause the disease.

5. Mechanisms of Pathogenicity: The pathogen should have factors that allow it to contribute to the disease state (i.e. LPS)

30
Q

What are the Layers of Epithelium?

A
  1. Oral epithelium
  2. Crevicular/Sulcular epithelium
  3. Junctional epithelium
31
Q

What are Desmosomes?

A
  • Filaments that go into cytoplasm of each cell
  • Between epithelial cells
  • Attachment plaque from each cell
  • Tonofilamets insert from each cell = brush-like

Two dense attachment plaques (one from each adjacent cell) into which tonofibrils insert from each cell, and an intermediate electron-dense line in the extracellular compartment. Tonofilaments (cytoskeleton of keratin proteins) radiate in brush-like fashion from the attachment plaques out into the cytoplasm of the two adjacent cells

32
Q

What are Hemidesmosomes?

A
  • Only go 1 direction
  • Connects Junctional Epithelium to tooth
  • Connects Epithelium to CT
33
Q

What are Intrinsic Cementum Fibers made from?

A

Cementoblasts

34
Q

What are Extrinsic Cementum Fibers made from?

A

PDL fibroblasts

35
Q

What is Primary Acellular Cementum

A
  • Cells of the dental follicle differentiate into cementoblasts
  • Cells of HERS secrete enamel matrix proteins which cover the dentin matrix being formed by odontoblasts;
  • cementoblasts secrete type I and III collagen fibrils onto that enamel matrix layer; as this fine fibrillar cementum calcifies, it forms a uniform cell-free cementum called “primary acellular cementum”
  • The fibers in this cementum are called “intrinsic fibers of cementum”.
36
Q
A
37
Q

What is the process for how Extrinsic fibers of cementum are formed?

A
  • As the cementum matrix thickens and calcifies, it begins to entrap collagen fiber bundles from the PDL which are called “extrinsic fibers of cementum”
  • On the bone side, PDL fibers are also being trapped in calcifying bone matrix.
  • The insertion of the PDL fibers into bone and cementum are called “Sharpey’s fibers”.
38
Q

Where are Sharpey’s Fibers most numerous during cementum formation?

A

Sharpey’s fibers are more numerous and smaller on the cementum side than on the bone side – important in remodeling because occlusal forces are more evenly distributed on cementum side (most remodeling due to occlusal forces occurs in bone since forces are more concentrated)

39
Q

What is Secondary cementum and how does it form?

A
  • Once the tooth erupts and meets an opposing tooth, primary cementum formation generally stops. Secondary cementum formation occurs over the primary cementum
  • Forms fairly quickly, so cells become entrapped (“cellular cementum”) layers of cellular cementum often alternate with layers of acellular cementum, since cementum matrix deposition goes thru spurts of fast formation followed by slow formation.
  • Continues to form throughout life, especially at apex of root (may compensate for enamel attrition over time)
40
Q

Where is Secondary Cementum the thickest?

A
  • Thickest in the more apical region of the root because that part of the root is still forming after the tooth contacts its opposing tooth)
41
Q

What is Afibrillar Cementum?

A
  • Only found up near the CEJ and overlapping onto enamel. It is formed late in the process and usually doesn’t last long because it is very thin.
42
Q

How does the Alevolar Ridge change after extraction?

A
  • Decrease by 50% (Schropp)
  • 2mm less reduction in ridge width and buccal height and 1mm less reduction in lingual ridge height (Avila-Ortiz)
43
Q

What are the Ramfjord teeth?

A

3,9,12,19,25,28

44
Q

What branch does the Maxillary Artery come from?

A

External Carotid Artery

45
Q

What are the 3 portions of the Maxillary Artery?

A
  • Mandibular/bony portion: inferior alveolar artery (gives rise to mental, incisor, mylohyoid)
  • Pteygoid/muscular portion: buccal artery
  • Pterygomaxillary/pterygopalatine portion: nasopalatine, greater/lesser palatine, posterior superior alveolar artery, infraorbital (gives rise to mid and ant superior alveolar arteries)
46
Q

What are the 3 arteries run through Maxillary sinus?

A

1. PSA

2. Infraorbital

3. Posterior Lateral Nasal Artery (this one possibly encountered during lat window)

47
Q

What is the Distance of the greater palatine neurovascular bundle in Shallow, Average, and Deep Palate?

A

(Reiser)– Measured from the crest

1. Shallow: 7mm

2. Average: 12 mm

3. Deep: 17mm

48
Q

When we say, “the periodontium”, what tissues are we talking about?

A

1. Gingiva

2. Connective Tissue Attachment (Gingival attachment to the tooth)

3. PDL

4. Alveolar Bone

49
Q

What causes Gingival Stippling?

A

Invaginations of the oral epithelium into the underlying connective tissue

50
Q

If you look at the gingival connective tissue just under the epithelium– what are the two layers of connective tissue?

A

The Papillary layer which extends up between the epithelial rete pegs (less dense fibers), and the Reticular layer (more dense fibers) under the papillary layer

51
Q

How are epithelial cells “attached” to underlying CT?

A
  • Via a basement membrane and anchoring fibrils
  • Basement membrane is called “basal lamina” at electron microscopic level, and has two layers
    • Lamina lucida closest to epithelial cell (translucent on EM) – made of laminin
    • Lamina densa (closest to underlying CT) – made of type IV collagen
  • Anchoring fibrils (collagen, mainly type VII) come up from underlying CT and anchor the lamina densa to the CT
52
Q

Describe the blood supply to the periodontium (PDL, Alveolar Bone, and CT)

A
  • Blood comes from superior and inferior alveolar arteries into the PDL, the alveolar bone and along the surface of the periodontium
  • Blood vessels extend into gingival CT and go up into CT papillae right under epithelium where there are extensive capillary loop
  • Gingiva is an end-organ
  • Extensive vascular anastamoses allow rapid healing after injury (e.g., incisions, etc.)
53
Q

Distinguish between woven bone and lamellar bone

A

Woven bone: usually has lots of calcified collagen fibers in it; woven bone is immature bone

Lamellar bone: more mature bone; appears like “layers” of bone; forms the compact bone on the buccal and lingual surfaces of the alveolar process

54
Q

What is Trabecular Bone?

A
  • B/W the buccal and lingual cortical plates (if the alveolar process is thick enough;
  • If it’s very thin, you may have only compact cortical bone and no trabecular bone)
  • Cortical bone is almost always lamellar bone (mature); trabecular bone is combination of woven bone (newly formed and less mature) and lamellar bone (more mature)
55
Q

What is the Lamina Dura?

A

Radiographic term for radiodense line along socket wall and over crest of alveolar plate

56
Q

How does the enamel meet the cementum at the CEJ?

A
  • About 60-65% of cases have a thin layer of afibrillar cementum lying over the enamel - Overlay
  • About 30% of teeth have a butt joint where enamel meets cementum
  • About 5% of cases have a “gap” between enamel and cementum (so there is dentin right at the “CEJ”)
57
Q

Describe environmental surfaces of subgingival tooth surfaces

A
  • Bathed in GCF as opposed to saliva
  • GCF is rich source of IgG and IgA antibodies
  • GCF is an inflammatory exudate rich in antibodies
58
Q

What is Saliva?

A

A turbulent environment with no fixed surface for microorganisms to reside

59
Q

Is periodontal disease mainly caused by endogenous or exogenous bacteria?

A

Endogenous – most forms of gingivitis and periodontitis are caused by members of the normal flora

Exogenous is NOT native to oral cavity

60
Q

What are some examples of Virulence Factors/Modes of Attachment (MOA)

A

1. Fimbriae, pili, fibrillae

  • Attachment, prevention of phagocytosis

2. Capsule, exopolysaccharide, glycocalyx

  • Attachment, prevention of phagocytosis, protection from complement and immune system

3. Peptidoglycan, muramyl peptides

  • Immunodilation, induction of inflammatory mediators

4. Endotoxin

  • Activation of inflammatory response, activation of cytokine production, induction of bone resorption

5. Proteolytic enzymes (collagenase, gelatinase, hyaluronidase, fibrolysin, immunoglobulin proteases, H2S, and volatile sulfur compounds)

  • Breakdown of host CT; host tissue invasion

6. Inorganic acids

  • Butyric acid, propionic acid—host cell toxicity

7. Superoxide dismutase

  • Breakdown of oxygen product, protecting anaerobes
61
Q

What is a Biofilm

A

Plaque and community of pathogenic microorganisms by enabling bacteria to act synergistically to provide nutrients to each other, safely remove waste products, and provide physical and chemical barriers to avoid the host immune defense or antimicrobial agent

Dental biofilm is the primary etiology of gingivitis

62
Q
A

Oral Boards Fall 2021 (2 decks)

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