Implant biology Flashcards

1
Q

PDL natural vs implant

A

all fiber groups present in natural, none with implant

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2
Q

natural teeth PDL

A

*Periodontal fibers aIach from bone to root in multiple
directions
*Periodontal Ligament act as shock absorber
*Connective tissue fibers attach to teeth

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3
Q

implant PDL?

A
  • Direct bone to implant contact (osseointegration)
  • Ankylosis
  • Peri-implant fibers parallel cuff, oriented longitudinal
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4
Q

Supracrestal tissue attachment components and measurements

A
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5
Q

implant epi cell attatchement

A

attatched via hemidesmosomes

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6
Q

parallel cuff

A
  • Collagen fibers do not insert into the implant but creates a cuff around the implant
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7
Q

Difference in Blood Supply with implants
* Blood supply by?
* inflammatory response?
* Capillaries?

A
  • Blood supply by terminal branches of large vessels
    from periosteum.
  • More inflammatory response than gingival Bssues
  • Fewer Capillaries
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8
Q

Teeth vs Implants
attatchment?
orientation of collagen fibers?
source of blood supply?
bio width?

A
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9
Q

bio width of implants

A

JE: 1.88mm
CT:1.05 mm
almost 3mm

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10
Q

JE length in implants

A

JE Length 1.3 to 1.8 mm (depends on the implant
design).
PDs may very based on implant design (and brand)

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11
Q

physiologic bone remodeling with implants

A

Once the implant is uncovered, vertical bone loss of 1.5 to 2 mm is evidenced apical to newly established implant-abutment interface.
After one year of Loading, up to 2 mm of bone loss is considered biologic bone remodeling and WNL

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12
Q

pathologic bone remoddeling with implants

A

Baseline X-ray to evaluate progressive Bone Loss.
>= 2mm after the first of function is pathologic
>If you do not have a radiograph? PDs >= 6mm and BOP is pathologic
PERI IMPLANTITIS: characterized by inflammation in the peri-implant mucosa and progressive loss of supporting bone. Clinical sign of inflammation
is detected by bleeding on probings, while progressive bone loss is identified on radiographs”

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13
Q

How much bone is adequate? MD demension

A

at least 1.5 mm between teeth and implant (Esposito, 1993)
- 3 mm between 2 adjacent implants

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14
Q

implant placement for anterior papilla

A
  • 3-4 mm deeper than adjacent margin for papilla in anterior teeth
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15
Q

adequate bone in BL demension

A

As bone thickness approached 1.8 - 2 mm, bone loss decreased significantly and some evidence of bone gain was seen

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16
Q

BUCCO-LINGUAL demensions (Posteriors)

A

*non linear correlation between buccal ridge width and the resorption
*2 mm threshold established to account for non linearity . Significantly greater resorption when the ridge width < 2 mm
* At least 1 mm buccal and lingual needed.

17
Q

subcrestal placement

A

recommended to place implant beneath bony crest about .5mm
hides moderately rough surface from microbiota

18
Q

Platform Switching

A

Concept of placing an abutment of a narrower diameter on the implant of a wider diameter to preserve alveolar bone levels at the crest of a dental implant

19
Q

how does platform switching work

A

-Shifts the inflammatory cell infiltrate inward and away from the adjacent crystal bone
-Maintains the supracrestal attachment
-Increases distance of implant-abutment junction from the crystal bone
-limits possible interface of bone with micromovements

20
Q

The influence of Microgap at two-part
implants

A

Inflammatory cell infiltrate was consistently present at the level of the interface between the two components, the bone crest was consistently located 1-1.5 mm apical of the microgap.
* Inflammatory Infiltrate was due to bacterial contamination
* Placement of two-part implants at different levels in relation to the bone crest resulted in different amounts of bone loss.

21
Q

microgap and bone loss flow chart

A
22
Q

Kera2nized Tissue and Implants

A

Implant sites with a band of <2 mm of KT were shown to be more prone to brushing discomfort, plaque accumulation, and peri-implant soft tissue inflammation when compared to implant sites with ≥2 mm of KT.

more keratinized tissue the better

23
Q

how can we increased the amount of KT

A

tissue grafts