Sweep 1 Flashcards

1
Q

Osseointegration:

A

The direct attachment or connection of vital osseous
tissue to the surface of an implant, without intervening
connective tissue.

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2
Q

Rigid fixation –

A

Clinical term to define osseointegration

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3
Q

Various steps used in surgical procedure:

A

1- Incision

2- Mucoperiosteal flap elevation

3- Preparation of a bed in the cortical and 		    spongy bone (osteoctomy)

4- Insertion of the titanium device
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4
Q

Initial implant stability –

A

press-fit implant placement

Lateral displacement of bone tissue and the tight
contact at the cortical bone level.

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5
Q

Surgical trauma –

A

Initiation of wound healing.

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6
Q

Ultimate implant goal:

A

The implant to become “anchylotic” with the bone

The establishment of a mucosal attachment

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7
Q

24 hrs healing –

A

Resorption at the cortical bone.
Woven bone formation in the spongious bone.
Blood clot formation.
Proliferation of vascular structures into newly
forming granulation tissue.

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8
Q

1 week healing-

A

Reparative macrophage and undifferentiated
mesenchymal cells.
Modeling at the apical trabecular region and
at the “furcation sites” of a screw-shaped
implant.

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9
Q

2 weeks healing –

A

New bone formation can be detected at

the “furcation sites” of the implant surface.

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10
Q

Up to 6 weeks healing –

A

Callus formation and lamellar

compaction within woven bone.

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11
Q

During healing, you see

A

Temporary decrease in implant stability
Plateau effect in implant stability after 6 weeks and
Enhanced bone formation around implant.

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12
Q

“Jumping distance” concept –

A

The distance that can be filled by new bone between the implant and the remaining host bone.

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13
Q

Ideal tolerable distance =

A

20-40 microm

A larger gap does not heal well.

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14
Q

TPS=

A

Titanium Plasma Sprayed

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15
Q

SLA=

A

Sand Blasted Acid Etched

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16
Q

HA=

A

Hydroxyapatite

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17
Q

TCP=

A

Tricalcium Phosphate

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18
Q

Titanium is mostly used as

A

Ti-6Al-4V alloy.

Covered with a layer of titanium dioxide.

Biologically inert.

Increase in thickness with time.

Porosity increases surface area.

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19
Q

Bone response is stronger to surfaces with

A

irregularity values of 1.0-1.5 microns.

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20
Q

An implant should be surrounded with a minimum of

A

1 mm alveolar bone thickness.

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21
Q

Minimum bone thickness between 2 implants should

be

A

3 mm (implant surface to implant surface) and

22
Q

minimum bone thickness between an implant and

a tooth should be

A
4 mm (from root surface to implant 
surface).
23
Q

Coronal part of an implant should be placed

approximately

A

5 mm apical to the adjacent CEJ.

24
Q

Obtaining maximum parallelism between

A

implants and
teeth is critical.

Implants do not have periodontal ligament and cannot
tolerate horizontal forces.

25
Q

An implant can be placed with a maximum of

A

20 angle.

26
Q

The transmucosal attachment-

Two parts:

A

Barrier epithelium
(2 mm long)
Zone of connective tissue
(1-1.5 mm high)

Collagen fiber bundles parallel
to implant surface.

27
Q

Zone that is adjacent to implant surface is rich from

A

fibroblast but poor from blood vessels.

28
Q

Zone that is in lateral direction and continuous with

the first zone has fever

A

fibroblasts but it is rich in

collagen fibers and blood vessels.

29
Q

Blood supply coming only from

A

supraperiosteal blood

vessels.

30
Q

Two stage implant placement sx=

A

submerged tech.

31
Q

One stage implant placement sx=

A

non-submerged tech.

32
Q

Microgap =

A

Micro space that exists
between implant and abutment.

It is generally located at alveolar
crest.

33
Q

Biological width concept and dental implants-

A

A biological width exists around unloaded and loaded
nonsubmerged one-part titanium implants.
It is approximately 3 mm.

34
Q

Clinical parameters used to evaluate peri-implant health:

A

1- Absence of mobility
2- Radiographic examination
3- Absence of bone loss 0.2 mm/year following the first
year
4- Absence of any pain, complain and infection
5- Functional and esthetic acceptance of implant
supported restoration by both patient and doctor
6- A success rate of 94-98% following 5 years and
90-94% following 10 years

35
Q

3 available techniques to evaluate dental implants:

A

1- Peri-implant probing
2- Existence of mobility
3- Radiographic examination

36
Q

RFA (Resonance Frequency Analysis)

A

Mechanically, the resonance frequency of an object

is strongly correlated to the boundary constrains of the structure.

37
Q

A.a is associated with LAP

A
Facultative anaerobe, nonmotile.
Virulence factors:
Leukotoxins: kills PMNs and MΦ
LPS: activates cells to produce PGs, IL-1, TNF-
Collagenases: degrades collagen fibers 
Immunosuppressive factors : 
Lymphocyte supprressing factors
Chemotactic suppressing factors 

Translocate across the JE
Invade the CT

38
Q

P. gingivalis

A
Anaerobe, nonmotile, G-. 
Virulence factors: 
Proteinases: Gingipains, Collagenases 
LPS: activates cells to produce PGs, IL-1β, TNF-α 
Inibits IL-8: ↓ chemotaxis of PMNs.
39
Q

Diagnosis of AP

Quesations to answer

A
Microbiologic diagnosis
A.a., P.g., both, neither one?
Biochemical analysis
Crevicular PGE2 levels largely increased?
IgG2 titers against A.a.?
40
Q

Major microbial virulence factors

Immunostimulatory molecules

A

LPS (endotoxin) from Gram-negative bacteria, disrupt host response
Lipoteichoic acids from Gram-positive bacteria
Gingipains (Arg-specific protease)
Formylpeptides (stimulate leukocyte chemotaxis) - chemotactic factors for phagocytic leukocyytes. They guide leukocytes to source of infection. Other surface antigens on pathogenic bacteria
Other surface antigens

41
Q

Complement system

Induces

A

bacterial lysis
Promotes phagocyte recruitment (chemotaxis)
Promotes phagocytosis by opsonization of bacteria
Helps activate mast cells, which increases vascular permeability

42
Q

Oral mucosa produces

A

anti-microbial peptides (e.g., defensins)

43
Q

Oral epithelium produces

A

pro-inflammatory cytokines

44
Q

IL-1ß and TNF-α are universal signals of

A

infection that help recruit inflammatory cells

45
Q

IL-8 attracts

A

neutrophils in the early stages of infection

46
Q

In gingival crevicular fluid and saliva – secretory IgA helpful antibody that prevents

A

certain bacteria adhering.

47
Q

Von Ebner’s glands – release

A

antimicrobial peptides (similar to histatins).

48
Q

Toll-like receptors (TLRs)

A

Major role in induction of innate immune response
Recognize conserved microbial-associated molecular patterns (including LPS, lipoteichoic acid and flagellae)
Expressed by all cells, including epithelial cells, PMNs, monocytes and macrophages
TLRs signal for cells to produce cytokines, chemokines, antimicrobial peptides, nitric oxide and eicosanoids

49
Q

Biological activities of LPS (endotoxin)

A
Complement activation
PMN activation
Macrophage activation
B-cell mitogen activity
Stimulation of bone resorption
Stimulation of prostaglandin synthesis
Induction of Tumor Necrosis Factor (TNF-α)
50
Q

Mediators of innate immunity: Cytokines

Pro-inflammatory activity:

A

IL-1β, TNF-α

51
Q

Mediators of innate immunity: Cytokines

Chemotactic activity:

A

IL-8 – neutrophil attractor.