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Perio Final > Sweep 1.3 > Flashcards

Sweep 1.3 Flashcards

1
Q

Important acute phase proteins

A 
Complement components: opsonization, lysis, chemotaxis (CTX) 
Protease inhibitors (2-macroglobulin)
C-reactive protein (CRP):  opsonization
Fibrinogen:  coagulation factor, CTX
Plasminogen:  degrades blood clots
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2
Q

S. sanguis and P. gingivalis can induce

A

thrombo-embolic events (Herzberg & Meyer, 1996). This action is mediated by collagen-like platelet aggregation associated proteins made by bacteria.

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3
Q

A. actinomycetemcomitans LPS enhances

A

foam cell formation by macrophages incubated in vitro with LDL (Morishita et al, 2013)

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4
Q

Gingipains from P. gingivalis up-regulate expression of

A

angiopoetin 2 (pro-inflammatory action) and down-regulate expression of antiopoetin 1 (anti-inflammatory) in human aortic smooth muscle cells. This change in gene expression increases migration of smooth muscle cells and promotes atherosclerosis (Zhang et al, 2015)

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5
Q

Subjects with severe periodontitis are more likely to have elevated

A

HbA1c levels than subjects in health or with moderate periodontitis.

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6
Q

If you remove plaque and lesion, the signal for turning on basal layer of epithelium

A

goes away. You stop producing pro-inflammatory cytokines.

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7
Q

Early lesion

Accumulation of

A

lymphoid cells immediately subjacent to JE

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8
Q

Early lesion

Cytopathic alteration in

A

resident fibroblasts

Further loss of collagen network

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9
Q

Early lesion

Early proliferation of

A

basal cells of JE

Inflammatory changes are clinically evident

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10
Q

Established lesion histopathology

A

Increased swelling clinically evident
Increased fluid exudation, leukocyte migration
Plasma cells increase around blood vessels and in coronal CT
Collagen loss continues as infiltrate expands

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11
Q

Established lesion

In addition to macrophages and serum proteins,

A

T and B cells and plasma cells are present

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12
Q

Established lesion

Activated T cells produce

A

cytokines (IL-2, 3, 4, 5, 6, 10 and 13, TNF-) and chemotactic substances (MCP, MIP and RANTES)

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13
Q

Established lesion

Plasma cells produce

A

Ig and cytokines (IL-6 and TNF-)

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14
Q

Established lesion

Fibroblasts produce

A

MMPs and TIMPs

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15
Q

TIMP =

A

tissue inhibitor metalloproteinase – counter proteinaise, balance still shifts to protenolysis.

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16
Q

Conversion of JE to PE

A

The JE and sulcular epithelium proliferate, migrate deep into CT
The sulcus deepens and the coronal portion of the JE is converted into permeable pocket epithelium (PE)
The PE is not attached to tooth surface
The PE is loaded with PMNs

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17
Q

Switch from T- to B-cell predominance signals conversion from

A

gingivitis to periodontitis

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18
Q

Destruction of CT attachment to root surface and apical migration of epithelial attachment indicates

A

first clinical sign of periodontitis.

19
Q

Bone destruction begins around

A

communicating blood vessels along crest of septum
Apical proliferation of PE into deep CT
PE is not attached to tooth

20
Q

Advanced lesion summary

A

Persistence of established lesion features
Increased proportion of plasma cells (~50%)
Extension of lesion into alveolar bone and PL, with significant bone loss
Continued loss of collagen fibers and matrix subjacent to PE
Formation of periodontal pocketing and apical migration of JE from CEJ

21
Q

Pregnancy, puberty and menopause

Estrogen affects

A

salivary peroxidases

22
Q

Estrogen increases

A

collagen metabolism, angiogenesis

23
Q

Pregnancy puberty and menopause

Increased

A

vascular response and inflammatory mediators

24
Q

Gingival inflammation

A

increases in puberty & pregnancy

25
Q

INcrease in gingival bleeding during

A

menstrual cycle in women with gingivitis

26
Q

Pregnancy

Effects on microbiota

A

 in P. intermedia
Naphthoquinones from steroids support growth of P. i.
 in spirochetes

27
Q

Pregnancy

Effects on host

A

 in vascular permeability, resulting in  gingival exudate
decrease in keratinization
decrease in PMN chemotaxis and phagocytosis
decrease Ab and T-cell responses

28
Q

Pregnancy

Periodontal treatment

A

Best during 2nd trimester

Best to avoid use of antibiotics during pregnancy

29
Q

Ailing implant

A

Peri-implant mucositis

Peri-implantitis

30
Q

Failing implant

A

Peri-implantitis

31
Q

Failed implant

A

Peri-implantitis with mobility and complete loss of osseointegration

32
Q

Peri-implantitis and peri-implant mucositis

A

Definitions (Consensus report of the 1st European Workshop on Periodontology, 1994)
Peri-implant mucositis: Reversible inflammation of the mucosa surrounding the implant.
Presence of bacterial plaque and calculus.
Edema, redness and mucosal hyperplasia.
Bleeding on probing.
Exudate or pus formation on occasions (gingival microabscess).
No radiological evidence of bone resorption.
Peri-implantitis: Inflammatory reactions associated with loss of supporting bone around an implant in function

33
Q

Peri-implantitis in humans: histology

A

Peri-implantitis lesions are characterized by the presence of numerous neutrophils in the tissue surrounding the implant
In peri-implantitis, there is direct contact between plaque on the implant surface and inflamed connective tissue.
These features are not seen in periodontitis

34
Q

Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)

Class 1

A

Slight horizontal bone loss with minimal peri-implant defects

35
Q

Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)

Class 2

A

Moderate horizontal bone loss with isolated vertical defects

36
Q

Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)

Class 3

A

Moderate to advanced horizontal bone loss with broad, circular bony defects

37
Q

Classification of peri-implantitis(Jovanovic 1990, Spiekermann 1991)

Class 4

A

Advanced horizontal bone loss with broad, circumferential vertical defects, as well as loss of the oral and/or vestibular bony wall

38
Q

Class 1

A

Surgical reduction of pocket depth, thinning of mucosal flaps and apical repositioning of flaps at a bone edge level, using the corresponding suture technique.
The implant surface is cleaned and decontaminated.
Implantoplasty is only performed if threads are exposed.

39
Q

Class 2

A 
Similar to class 1, but repositioning is performed more apically, leaving more implant surface exposed, thus requiring an implantoplasty.
If local vertical resorption has three or more walls, this bone defect is restored using classical GTR techniques. 
In cases where the defect involves one or two walls, osteoplasty or bone leveling is performed to favor soft tissue repositioning, to fulfill self-cleaning criteria.
40
Q

Class 3 and 4

A

In peri-implantitis class 3 and 4, the presence of vertical defects almost always requires the use of GTR techniques.

41
Q

Good prognosis:

implants

A

25% attachment loss and/or class I furcation involvement
Adequate remaining bone support
Adequate possibilities to control etiologic factors and establish a maintainable dentition,
Adequate patient cooperation
No systemic environmental factors or well controlled systemic factors.

42
Q

Implants

Fair prognosis:

A

25-50% attachment loss
grade I or easily accessible Grade II furcation involvement,
adequate maintenance possible
Few systemic complications

43
Q

Implants

Poor prognosis:

A

> 50% attachment loss
Class 2 tooth mobility
Inaccessible grade II furcation involvements, grade III furcation
difficult-to-maintain areas and/or doubtful patient cooperation,
presence of systemic/environmental factors.

44
Q

Implants

Hopeless prognosis:

A

> 75% attachment loss
Tooth mobility 2+
grade II and III furcation involvements,
difficult-to-maintain areas and/or doubtful patient cooperation,
Root proximity

Perio Final (8 decks)

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