Perio Sweep 1.1 Flashcards

1
Q

TFO and inflammation are

A

separate processes
No enhanced attachment loss

NO co-destruction

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2
Q

Co-destructi0n: TFO and inflammation

A

at same site
Lesions merge
Enhanced attachment loss
Co-destruction

Inflammation in same area of TFO: co-destruction and accelerated bone loss
Inflammation reaches apical to the crest of bone

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3
Q

Methods of Occlusal Therapy: Irreversible

A
Intracoronal splints (require tooth preparation)
Occlusal adjustment by selective grinding
Orthodontics
Orthognathic surgery
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4
Q

Occ. Trauma and PD: Evidence

Periodontitis (inflammation) must be present for

A

attachment loss to occur

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5
Q

Occlusal trauma in the absence of periodontitis may be

A

reversible and result in adaptation (a mobile but otherwise healthy tooth

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6
Q

No repair can occur unless

A

inflammatory periodontal disease is first resolved

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7
Q

Occlusal trauma superimposed on an existing periodontitis may under certain conditions

A

accelerate attachment loss

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8
Q

Occlusal therapy in conjunction with periodontal treatment is indicated when

A

occlusal trauma is present

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9
Q

Occlusal therapy should not be done until

A

inflammatory PD is first controlled during initial periodontal therapy (helps decrease inflammation)

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10
Q

Occlusal therapy is especially indicated prior to

A

periodontal regenerative therapy

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11
Q

Occlusal adjustment is not justified in the absence of

A

periodontal disease as a preventive measure

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12
Q

Primary stability=

A

stability of the implant at the time of placement (mechanical interlocking mechanism between a screw and bone surface)

- Bone density
- Implant fixture design
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13
Q

Healing at the interface=

A

Bone formation and remodeling
[Conventional healing time:
*Mandible…. 3 months
*Maxilla …. 6 months]

The effect of functional implant loading on bone formation

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14
Q

Functional Loading of the Implant

A
Immediate Loading (at the time of placement)
 Early loading (before conventional healing time)
 Late loading (following 3 or 6 months
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15
Q

Restorative Design

A

Single tooth restoration
Multiple unit fixed type restoration
(splinted versus individual crowns)
Full mouth fixed type implant supported restoration
Full mouth removable type implant supported restoration

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16
Q

Implants in excessive occlusion

A

Porcelain Fracture
Implant to abutment (screw loosening or fracture)
Implant fixture fracture

Increasing mobility of adjacent teeth

Eruption/malocclusion etc of adjacent teeth (observed following functional loading of the dental implant)

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17
Q

Periodontal Tactile Perception and Peri-implant Osseoperception

A

Tooth extraction&raquo_space;> Sensory amputation
Myelinated fiber content of the inferior nerve reduced by 20%
Presence and potential function of sensory nerve fibers in the bone and peri-implant environment
Gradual increase in free nerve endings close to implant-bone interface during healing
Existing mechanoreceptors in the periosteum

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18
Q

“Tactile Sensibility” and “Thickness Discrimination”

A

Sensory feedback through receptors localized within pdl (viscoelasticity) and within bone (elasticity)…
Necessary for fine tuning of jaw and limb motor control.
Detection thresholds of 20 m of thickness in between antagonist teeth and 1-2 g upon tooth loading.
After implant placement, detection thresholds of 50-100 m of thickness and 50-100 g upon tooth loading.

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19
Q

Functional occlusal forces and implants(summary from various studies)

Loading time depends on:

A
  • Primary stability of the implant
    • Implant design
    • Restorative design
    • Presence/absence of risk factors
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20
Q

Functional (and well controlled) loading may increase

A

bone to implant contact BUT

Hundred percent bone-implant surface contact is NOT possible.

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21
Q

Occlusal trauma is a ——— for periodontal disease but …

A

secondary etiological factor

it can be a primary etiological factor for peri-implant disease.

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22
Q

Bruxism: LONGER AND WIDER

A

DENTAL IMPLANTS TO TOLERATE CHALLENGES !!!

SURROUNDED WITH THICK BONE SUPPORT !!!

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23
Q

Lateral loads induced

A

high bone strain and implant stress than vertical loads.

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24
Q

Periodontal disease is currently diagnosed almost entirely on the basis of its

A

clinical manifestations

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25
Q

Assessment of host resposne

A

Biochemical analysis as part of periodontal diagnosis
Source of samples:
GCF, saliva, and serum (blood)

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26
Q

Genetic Analysis (only for research)

A

There is a genetic susceptibility to periodontitis

Gene polymorphism as a risk marker for periodontitis

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27
Q

Diagnostic limitations

A

Lack of sensitivity and reproducibility
Probing depth: gingival inflammation, insertion force, placement and angulation, size, probing technique, probe calibration, presence of subgingival calculus, overhanging restorations

28
Q

Limited sensitivity in small bone change

A

– Changes in bone can be identified by eye only after 30% to 50% of the bone mineral has been lost (Subtraction
radiography: detect bone density change as low as 5 %)
No value in evaluating disease activity or progression

29
Q

Ultrasonic periodontal probing

A

Ultrasonic periodontal probe uses a hollow tapered tip that is filled with water for coupling of the ultrasonic beam into the tissues (non-invasive)

30
Q

Conventional radiographs (PA; Pano) are very

A

specific, but lack sensitivity

31
Q

Recently, dental CBCT has been introduced in periodontology for the detection of

A

periodontal defects in in vitro settings

32
Q

CBCT is promising for

A

periodontal applications, especially for intrabony defects, dehiscence and fenestration defects, periodontal cysts, furcation defects and thickness of palatal masticatory mucosa

33
Q

The sensitivity of a diagnostic test refers to the probability of the test being

A

positive when the disease is truly present

34
Q

The specificity of a diagnostic test refers to the probability of the test being

A

negative when the disease is not present

35
Q
  1. Bacterial Culturing
A

Gold standard (reference) method
Assess for antibiotic susceptibility of microbes
Can only grow live bacteria: strict sampling and transport conditions are essential
Some putative pathogens are fastidious and difficult to culture
Sensitivity is low: detection limits for selective and nonselective media average 104 to 105 bacteria
Sophisticated equipment and experienced personnel required; relatively time-consuming and expensive

36
Q

Fastidious microorganism – microorganisms that will grow only if

A

special nutrients are presence

37
Q
  1. Direct Microscopy
A

Alternative to culture methods
Dark-field or phase-contrast microscopy
Morphology and motility of bacteria in a plaque sample
Most of the main putative perio pathogens are non-motile (so it is difficult to identify)

38
Q
  1. Immunodiagnostic Methods
A
Use Ab that targets specific 
	bacterial Ag
Direct and indirect 
immunofluorescent 
microscopic assay (IFA)
Able to identify pathogens 
   using a plaque smear
Used mainly to detect Aa and Pg
Comparable to bacterial culture
Does not require viable bacterial cells
39
Q
  1. Immunodiagnostic Methods
A
  • Cytofluorography (flow cytometry)
    complexity and cost prevent its wide use
  • Enzyme-linked immunosorbent assay (ELISA)
    Used primarily to detect serum antibodies to periodontal pathogens
    Membrane immunoassay (EvalusiteTM): chairside use to detect Aa, Pg, and Pi (detection limit of 105 for Aa and 106 for Pg)
  • Latex agglutination
    Based on the binding of protein to latex: latex beads are coated with species-specific antibody
    Currently these assays only for research purposes
40
Q
  1. Enzymatic Methods
A

Several putative periodontal pathogens such as Pg, Tf, and Aa possess in common a trypsin-like enzyme that hydrolyzes a substrate N-benzoyl-DL-arginine-2-naphthylamide (BANA).
Chair-side kit (PerioscanTM) was available in the 1990s
Inability to distinguish between individual bacteria
- It may be positive at clinically healthy sites
Negative result does not rule out the presence of other important periodontal pathogens

41
Q
  1. Molecular Biology Techniques
A

Analysis of DNA, RNA, and structure or function of protein from target microorganisms
Nucleic acid probes
Synthesized and labeled DNA (20-30 nucleotides)
Genomic DNA probe (whole DNA strand): significantly ↓ in sensitivity and specificity due to cross-reactivity to non-target microorganisms
16S rRNA – oligonucleotide probes (high sensitivity and specificity)
Checkerboard DNA-DNA hybridization
Whole genomic digoxigenin-labeled DNA
Up to 40 oral bacterial species in a single test
Not been generalized for diagnostic purpose
PCR
High sensitivity and specificity for the identification of target pathogens
PCR lower detection limit: 25-100 cells (Culture: 104-105 cells)
Unable to quantify pathogens accurately in clinical samples
Real-time PCR
Real-time PCR: good correlation between the fluorescent signal measured and the number of bacterial cells been used
Expensive and sophisticated technology in real-time PCR

42
Q

16s rRNA is like a

A

finger print: comparing certain locations on a 16s rRNA molecule with a database of known organisms allows the identification of organisms whose 16s rRNA signature is known.

43
Q

Real-time PCR is also known as

A

The quantitative real time polymerase chain reaction (qPCR). The Real-Time-PCR enables both detection and quantification.

44
Q

Hypophosphatasia (OMIM 146300, 241500, 241510) is an inherited disorder characterized by

A
defective bone and teeth mineralization and deficiency of serum and bone alkaline phosphatase (AP) activity. 
urinary phosphoethanolamine (PEA) is increased in hypophosphatasia. urinary inorganic pyrophosphate (PPi) level is also increased.
tissue-nonspecific alkaline phosphatase (TNAP) 
inorganic phosphate (Pi)
45
Q

Collecting GCF

A

Paper strips placed within the crevice for 30 seconds
Fluid volume can be quantified by Periotron®
Captured samples may not represent the entire periodontium
Selection of the teeth and sites is often difficult

46
Q

GCF

Currently > 65 components of

A

GCF have been evaluated
Host-derived enzymes and their inhibitors
Byproducts of tissue breakdown
Inflammatory mediators and host-response modifiers

47
Q

Intracellular destruction enzymes

A

Possible markers of active periodontal destruction

Released from dead or dying PMN/Neutrophils from periodontium

48
Q

Intracellular destruction enzymes: - Aspartate amino-transferase:

A

released during tissue destruction (cell death)

49
Q

Intracellular destruction enzymes: - Alkaline phosphatase:

A

a membrane-bound glycoprotein involved in maintenance of alveolar bone

50
Q

Intracellular destruction enzymes: - β-glucuronidase:

A

a lysosomal enzyme degrades proteoglycans and ground substance

51
Q

Intracellular destruction enzymes: - Elastase:

A

a proteolytic enzyme found in lysosomal granules of neutrophil

52
Q

Aspartate aminotransferase (AST)

A

Periogard Periodontal Tissue MonitorsTM (chair-side test kit)
A marked elevation in AST levels in GCF from sites with severe gingival inflammation
Inability to discriminate between sites with severe inflammation with or without attachment loss

53
Q

Alkaline phosphatase (ALP)

A

ALP in GCF are higher in diseased then healthy sites alkaline phosphate in disease.

54
Q

β-glucuronidase (βG)

Elevated βG in GCF from sites with

A

severe periodontal disease
High sensitivity and specificity when related to occurrence of clinical attachment loss
Good predictor for future periodontal breakdown

55
Q

Elastase

A

Periocheck® (chair-side test kit)

Positive correlation of elastase in GCF with clinical attachment loss

56
Q
Matrix metalloproteinases (MMPs)
Secreted by
A

fibroblasts and macrophages

57
Q

MMPS: Responsible for
the initial destruction of
periodontal ECM

A

remodeling and degradation of ECM components

58
Q

MMPS: Regulated by tissue inhibitors of

A

MMPs (TIMPs)

59
Q

MMPS: High MMP levels in GCF are at

A

significantly greater risk for progression of periodontitis

60
Q

GCF MMPs level reduces in response to

A

treatment

61
Q

MMP-2 (gelatinase A), MMP-9 (gelatinase B), MMP-8 (collagenase 2), MMP-13 (collagenase 3), and MMP-3 (stromelysin-1) involve in

A

in
the initial destruction of
periodontal ECM

62
Q

Destruction of collagen

A

The ECM of the periodontium is composed of collagen (predominant), proteoglycan (versican, decorin, biglycan, syndecan) and non-collagen proteins (elastin, fibronectin, laminin, osteocalcin, osteopontin, bone sialoprotein, osteonectin, and tenascin)
Elevated levels of hydroxyproline (breakdown from collagen), glycosaminoglycans (from matrix degradation) and osteocalcin & type I collagen (from alveolar bone destruction) can be found in the GCF from sites with periodontitis

63
Q

Bio-Plex Cytokine Assay

Incorporates

A

novel technology using color-coded beads, permits the simultaneous detection of up to 100 cytokines in a single well of a 96-well microplate
Are multiplex bead-based assays designed to quantitate multiple cytokines in tissue fluid including GCF

64
Q

OPTICAL SPECTROSCOPY

Infrared (IR) Spectroscopy

A

Vibrating covalent bonds of organic molecules absorb a characteristic wavelength of IR light
The wavelength of light absorbed depends on the nature of the covalent bond (e.g., C=O and N–H), the type of vibration (e.g., bending and stretching), and the environment of the bond
The spectrum of absorbed light can be used to establish a molecular fingerprint of a tissue or fluid

65
Q

Diagnosis of Periodontitis Based on IR Spectra of GCF

A

Measure the total contents of GCF
IR spectroscopy can be used to characterized GCF from healthy, gingivitis, and periodontitis sites
Vibrations of peptide groups: C=O stretching (amide I band) and N–H bending (amide II band)
IR spectroscopy of GCF is reagent free, requiring only small sample volumes, requiring minimal training for