Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Perio Final > Ryan's Notes > Flashcards

Ryan's Notes Flashcards

1
Q 
Rapid onset of pain, interdental gingival necrosis (‘punched out’), bleeding
Pseudomembrane covers ulceration (white/graying slough)
Confined to interdental papilla/marginal gingiva
Young adults (ass. with smoking/stress)
Oral hygiene usually poor;  painful when brushing
Enlarged LN (esp. submandibular)
Fever/malaise not consistent characteristics
Increased salivation
A

Necrotizing ulcerative gingivitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Criteria:
Pain (CC); Papilla necrosis - “punched out”; Bleeding
Attachment loss
Other possible features:
Pseudomembrane & halitosis (foetor)
Oral hygiene usually poor; painful when brushing
Enlarged LN (esp. submandibular)
Fever/malaise not consistent characteristics
Increased salivation

A

Necrotizing ulcerative periodontitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q 
Aggressive causative agents:
Spirochetes (Treponema) → main pathogen
Fusobacterium; P. intermedia
CMV; HIV
Host factors:
Immunosuppression 
Pre-existing gingivitis; poor oral hygiene; history of previous NPD
Stress/smoking
A

Etiology of NPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

necrosis of epithelium & hyperemic CT; PMN infiltration
oBacterial zone; PMN rich zone; necrotic zone; spirochetal infiltration zone
Diagnosis via clinical presentation
oTriad of Sx +/-CAL

A

Histopathology of NPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Differential diagnosis of NPD

A

primary herpetic gingivostomatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

affects entire oral mucosa
Children present with oral vesicles; fever
oDesquamative lesions ⇒ gingiva/mucosa; immunologic; adults; pain/burning
Therapy:
oDebridement & oral rinses (CHX) & Atbx (metronidazole)
oSurgical therapy (defect elimination)

A

Primary herpetic gingivostomatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What kind of periodontal abscess?
oEtiology ⇒ irritation from foreign bodies forcefully embedded into previously healthy tissue
oGenerally limited to marginal gingiva or interdental papilla
oSudden onset of localized painful expanding lesion

A

Gingival abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What kind of periodontal abscess?
oLocalized purulent inflammation of periodontal tissues
Localization occurs when drainage thru pocket impaired
oOften occurs in molar sites
oAss. with pre-existing periodontitis (deep pockets)

A

Periodontal abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

oExacerbation of chronic lesion
Untreated patients & maintenance pts (recurrent infxn)
oPost-therapy abscess
Following SRP (calculus) or surgical therapy (calculus; foreign body)
oPost-antibiotic abscess (super-infxn)

A

Other reasons for periodontal related abscesses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What kind of abscess?
Foreign body impaction (oral hygiene devices; food particles)
Root morphology alterations
Iatrogenic (endodontic perforations)
External root resorption; cemental tears
Complications:
oTooth loss
oSystemic infections (dissemination via bacteremia or iatrogenically during therapy)

A

Non-periodontitis related abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Etiology ⇒ Periodontal flora (P. gingivalis 50-100%)
Diagnosis:
oPain, swelling, redness & suppuration (either spontaneous or after pressure)
Ass. with deep pocket, BOP, mobility
oRadiographic widened PDL, bone loss
oFever, malaise, lymphadenopathy
Treatment:
oIrrigation with antiseptics & Drainage
oAtbx
oF/u 1-2 days after; definite treatment carried out after 1 week

A

Periodontal abscesses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Differential diagnosis of periodontal abscess?

A

oPeriapical endodontic abscess or endo-perio abscess (where periodontal abscess secondary)
oVertical root fx; osteomyelitis; periodontal cyst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Difference between periodontal abscess and endo abscess?

A
  • Periodontal abscess → tooth vital

* Endodontic lesion → tooth non-vital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

•Apical foramen
•Accessory canals
oFrequency increases towards apex
oMultiple directions - can lead to furcation
•Dentinal tubules
oCervical area where there is loss of cementum (can be natural)

A

Anatomic connection between pulp and PDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

•Non-vital tooth
oNecrotic pulp → disease extends to periodontal tissues
oAccessory canal can have effects on periodontum
•Endodontic therapy → resolution

A

Primary endodontic lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment
•Endo → partial resolution (treated first)
•Perio → complete resolution

A

Primary endodontic lesion with 2ndary perio lesion (combined lesion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  • Tooth vital
  • Perio therapy → defect resolution
  • If lesion reaches apical foramen → effects pulp (pulp necrosis follows)
A

Primary periodontal lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

True combined lesion

A

•Independent pulpal & periodontal pathologies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Effects of perio disease on the pulp

A
  • Perio disease (even severe) rarely leads to endo disease unless apical foramen involvement
  • Root surface defects, but no inflammatory changes in pulp
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

•Perio instrumentation can lead to root exposure (recession), cementum (dentin) removal, dentinal tubule exposure
•Pulp vitality unaffected
•Dentin hypersensitivity
Raid onset, sharp pain elicited by multiple stimuli
oPeaks at 1rst week, then subside (following SRP)
oPotential to become chronic
Treat chronic hypersensitivity by blocking dentinal tubule communication (special tooth paste; mechanical blockage; root canal last resort in severe cases)

A

Periodontal therapy effects on the pulp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

•Endo therapy complications → perforations & vertical fractures

A

Endo therapy effects on periodontium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

mechanism by which periodontitis influences systemic diseases
oTriggering factors → local reaction → mediators → secondary systemic reactions
Triggering factors:
•Infections; necrosis; surgery; neoplasia; radiation
Local reaction:
•Macrophages; fibroblasts; endothelial & other cells
Mediators - cytokines (TNFa; IL1; IL6; IFNy)
Secondary systemic rxn
•Fever & leukocytosis; complement activation; ↑ glucocorticoids
•↑ acute phase proteins (complement; a2-macroglobulin; CRP - opsonin; Fibrinogen; Plasminogen

A

Acute phase reaction cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

•Consistent association; strength of association
•Specificity of association (confounding factors weaken causal association)
•Correct time sequence ⇒ factor MUST precede disease
•Dose-response effect
oRisk of developing disease related to degree of exposure

A

Characteristics of a risk factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What disease is associated?
•Periodontitis → systemic inflammation → acute phase rxn → atherosclerotic changes & CHD
oInflammatory cytokines → stimulate atheroma development & acute phase response ( ↑ CRP & fibrinogen) increases coagulation → thrombosis → MI
•Periodontitis & ___ ⇒ share similar risk factors or common etiologic pathway
oOlder male pts; low SES: smokers & diabetics; HTN
•Major confounding factors in studies of association between __ & periodontitis
oSmoking; Age; Diabetes; SES
•Studies reveal:
oAssociation between poor oral health, tooth loss, periodontitis & CHD or MI
oPeriodontitis can influence atheroma formation
oAssociation between periodontal pathogens & vessel wall thickening
o1 study showed no association
•Biologic rationale - pathways that explain link between ___ & periodontitis
oPeriodontal bacteria effect on platelets
P. g. ⇒ can induce thromboembolic events
oInvasion of endothelial cells & macrophages by perio bacteria
Aa & P.g ⇒ can be found in atheromas
oPro-inflammatory mediators
CRP & fibrinogen elevated in periodontitis

A

Atherosclerotic vascular disease

AVD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

oSRP ⇒ reduces serum CRP & IL6 (Studies have not shown consistent reduction)

A

Periodontal therapy effect on cardiovascular disease biomarkers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

oImproved endothelial fxn & decreased intimal-medial thickness of arteries

A

Periodontal therapy effect on endothelial function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

oConsistent, but modest strength of association
oNon-specific association (bc confounding factors)
oTiming & sequence not assessed
oAssociation with degree of exposure
oBiologically feasible
No causal relationship

A

Strength of evidence for association between periodontal disease and AVD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

• Preterm low birth weight < 2.5 kg
•Periodontitis → inflammatory cytokines → Placental tissues release PGE2 inducing myometrial contraction & activated MMPs weaken membranes → Low birth weight (LBW) & Preterm birth (PTB)
•Joint EFP/AAP statement
oAssociation between adverse childbirth outcomes & systemic diseases somewhat modest
oPeriodontal therapy does NOT significantly reduce rates of ___ or ___

A

Association between periodontitis and adverse pregnancy outcomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

•Poorly controlled diabetics have more CAL than non-diabetics
oChronic hyperglycemia & AGE products → decreased PMN response & delays wound healing
•Severe periodontitis → higher risk of worsening glycemic control; higher HbA1c
•Joint EFP/AAP statement:
oReduction of HBA1c by SRP ⇒ has clinical impact similar to adding 2nd drug to diabetic regimen
oRCT with more subjects & greater follow up needed

A

Association between periodontitis and diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

•Respiratory pathogens can colonize dental plaque & serve as source of subsequent infection
•Association between periodontitis & hospital-acquired PNA emerging, but further study needed
•Oral hygiene likely to become important consideration for hospitalized pts at risk for PNA
•Joint EP/AAP statement:
oAss. between dental plaque & PNA appears stronger than for plaque & exacerbation of COPD
oMore studies of association needed

A

Association between periodontitis and risk of bacterial pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Odds ratio for what risk factor?

2.5-3.7

A

smoking, 2.5x to 3.7x more likely to have periodontitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Odds ratio for what risk factor?

2.8-3.4

A

diabetes 2.8-3.4x more likely to have periodontitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q
  • Microbiota → necessary, but not sufficient to cause disease
  • Inflammation → necessary, but not sufficient to cause disease
  • HIV/AIDS
  • Osteoporosis
  • Obesity
A

Risk indicators for periodontitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

oPrevious history of periodntal disease
oBOP; calculus; furcations
oRemaining teeth < 28 (minimum 21 needed for proper fxn)
oPeriodontal support in relation to age

A

Risk predictors for periodontal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

oExtent & severity of presenting disease
oLevel of oral hygiene
oInfrequent dental visits
oSmoking

A

Prognostic factors for periodontal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

variable contributing to cause of disease

A

etiologic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

variable associatied with increased chance of developing disease

A

risk assessment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

skin manifestations; perfect perio health with tooth mobility (widened PDL on XR)

A

scleroderma

39
Q

not an indicator of disease progression

oIndicates acute infection in pocket (possibly abscess)

A

suppuration

40
Q

when probe depth reaches or passes mucogingival jxn

oSulcus depth at or apical to mucogingival jxn

A

Mucogingival defect

41
Q

o Grade 0 ⇒ No catch
oClass 1 ⇒ slight catch & no radiolucency on XR
oClass 2 ⇒ catches & radiolucency of XR
oClass 3 ⇒ mandibular thru & thru furcation; maxillary 2 or 3 thru & thru
•CEJ to furcation 3 mm mesially; 4 mm buccally; 5 mm distally

A

Furcation involvement

42
Q

oClass I ⇒ > 1 mm of physiologic movement in 1 direction
oClass 2 ⇒ > 2 mm of movement in 1 direction or > 1mm in 2 directions
oClass 3 ⇒ tooth depressible (tooth movement in 3 axis)

A

Mobility

43
Q

oHorizontal bone loss (bone loss parallel to CEJ)
oVertical (angular) bone loss
Guided tissue regeneration possible depending of # of walls remaining
3 wall defect (3 remaining walls)
2 wall defect
1 wall defect

A

Different types of bone loss

44
Q

Which bone loss defect is the best to regenerate?

A

-3 walled defect

45
Q

Which bone loss defect is a lost cause?

A

1 walled defect

46
Q

What is another name for a 2 walled defect?

A

crater

47
Q

•Probing depths of 1-3 mm
•No h/o attachment loss & no current disease (sx of inflammation)
oIf history of CAL ⇒ generalized periodontal health on reduced periodontium

A

Clinical definition of health

48
Q

< 3mm probe depths; No history of CAL; inflammation
•Dental plaque-induced gingival swelling:
o< 3 mm probing depth & BOP
oRed & edematous soft tissue
oNo gingival recession
•Other forms (non-plaque induced):
oOften difficult to diagnose & treat
oInvolves systemic disorders & medications

A

Gingivitis

49
Q

< 3mm probe depths; No history of CAL; inflammation
•Dental plaque-induced gingivitis:
o< 3 mm probing depth & BOP
oRed & edematous soft tissue
oNo gingival recession
•Other forms of gingivitis (non-plaque induced):
oOften difficult to diagnose & treat
oInvolves systemic disorders & medications

A

Periodontitis

50
Q 
•Pain control
•Reduction &amp; resolution of gingival inflammation
oFull mouth BOP < 25%   (ideally < 10%)
oNo BOP indicates health for nonsmokers; does not indicate severity of disease
•Reduction of probing depths
oNo PD > 5 mm after SRP  (Ideally < 4mm)
•Elimination of open furcations
oFurcation involvement < 3mm
•Satisfactory function &amp; esthetics -  must meet pt expectations
•Control of risk factors
oProper plaque control
oSmoking cessation
oProper control of diabetes
A

Treatment goals

51
Q

What phase of treatment?
oCause-related therapy
Emergency treatment
Occlusal analysis & treatment of localized trauma from occlusion
oRemoval of hard & soft deposits
oRemoval of retentive factors
oPatient education & patient motivation (OHI) - very important
oExtractions; SRP; antibiotic therapy
oConcluded by re-evaluation (in 4-6 weeks)

A

Initial (hygienic) phase - etiotropic

52
Q

What phase of treatment?

oPerio surgery; implant surgery

A

Corrective phase

53
Q

oFrequency variable - 3 month recall
2 month recall for smokers
oPrevention of re-infection & recurrence
oAssessment & instrumentation of deepened, BOP+ sites
oCaries control & control of prosthetic restorations

A

maintenance phase - 3 month recall

54
Q

• Direct attachment of vital osseous tissue to surface of implant w/o intervening CT
•60% bone connection (100% Not possible)
oNo threshold determined for success vs. failure

A

Osseointegration = rigid fixation

55
Q

oImplant surface characteristics
oSurgical manipulation of alveolar bone
Based on anatomical location (mandible more compact than maxilla), augmentation techniques, & condensation (pushes bone to create space, pack bone rather than cut)

A

methods to increase osseointegration

56
Q

oBiocompatibility = titanium alloy (covered with layer of Ti-dioxide - biologically inert)
Increases thickness with time
oDesign of implant ⇒ root form
oSurface conditions of implant ⇒ rough vs polished
Porosity increases SA
Bone response stronger to surfaces with irregularity values of 1-1.5 um
oStatus of host
oSurgical technique at insertion - protect bone from heat; special drill used
oLoading conditions (immediate vs. early. vs late)

A

Background factors important for reliable osseointegration

57
Q
  • Lateral displacement of bone tissue & tight contact at the cortical bone level
  • Mechanical stability - ideal to have both compact & trabecular (compact more rigid, but trabecular has richer blood supply)
A

Initial implant stability - press fit implant placement

58
Q

•Incision → mucoperiosteal flap elevation → preparation of bed in cortical & spongy bone (osteoctomy) → insertion of titanium device

A

Steps used in surgical procedure

59
Q

•Goal ⇒ implant to become anchylotic & establishment of mucosal attachment

A

goal of surgical trauma- initiation of wound healing

60
Q

What stage of wound healing?
⇒ resorption at cortical bone; woven bone formation in spongious bone; blood clot formation; proliferation of vascular structures into newly forming granulation tissue

A

24 hrs

61
Q

What stage of bone healing?
reparative macrophages & undifferentiated mesenchymal cells; modeling at apical trabecular region & at ‘furcation sites’ of screw shaped implant

A

1 week

62
Q

What stage of bone healing?

new bone formation can be detected at ‘furcation sites’ of implant surface

A

2 weeks

63
Q

What stage of bone healing?
callus formation & lamellar compaction within woven bone
oTemporary decrease in implant stability - important consideration for loading
oPlateau effect in implant stability after 6 weeks & enhanced bone formation around implant

A

up to 6 weeks

64
Q
  • Distance that can be filled by new bone between implant and the remaining host bone
  • Ideal tolerable distance 20-40 um (larger gap does not heal well)
A

Jumping distance concept

65
Q
  • Accepted healing period for osseointegration is 6 months for maxilla; 3 months for mandible
  • Early loading often encouraged, but case based on loading factors
  • Bone will adapt as long as loading forces are not excessive
A

good time for implant loading

66
Q
  • Type 1 ⇒ rich in cortical bone (good for primary stability)
  • Type 4 ⇒ rich in trabecular bone (best blood supply)
  • Ideal ⇒ type 2 or 3
A

type of bone good for implants

67
Q

Where is the ideal implant localization?

A

at cingulum

68
Q

•Surrounded with minimum of 1 mm alveolar bone thickness
•Minimum bone thickness between 2 implants should be 3 mm (implant surface to implant surface) & minimum bone thickness between an implant & a tooth should be 4 mm(from root surface to implant surface)
•Coronal part of an implant should be placed 4 mm apical to adjacent CEJ
•Obtaining maximum parallelism between implants & teeth critical
oNo PDL, so cannot tolerate horizontal forces
oCan be placed with maximum 20° angle
•Transmucosal attachment:
oBarrier epithelium 2mm long
oZone of connective tissue 1-1.5 mm high
•Biological width & dental implants (non-submerged type - 3 mm)

A

Requirements for implant

69
Q

Collagen fiber bundles parallel to implant surface
Zone adjacent to implant surface high fibroblast, but low blood supply
Zone in lateral direction & continuous with first zone has fewer fibroblasts but richer collagen & blood supply
•Blood supply coming only from supraperiosteal blood supply

A

adjacent implant structures

70
Q

What technique of implant placement?

submerged

A

2-stage implant placement

71
Q

What technique of implant placement?

non-submerged

A

1-stage implant placement

72
Q

space that exists between implant & abutment; generally at alveolar crest

A

microgap

73
Q
  • Absence of mobility
  • Radiographic examination (need yearly PA)
  • Absence of bone loss > 0.2 mm/yr following first year
  • Absence of any pain, infxn
  • Functional & esthetic acceptance of implant supported restoration by both pt & doctor
  • Success rate of 94-98% following 5 yrs & 90-94% following 10 yrs
A

clinical parameters used to evaluate peri-implant health

74
Q
  • Peri-implant probing
  • Existence of mobility
  • Radiographic examination
A

3 techniques to evaluate dental implants

75
Q

What type of tissue to have around the implant?

A

Keratinized tissue/attached gingiva

76
Q
  • Age
  • Severity of disease
  • Systemic factors/smoking
  • Plaque/calculus & other local factors
  • Pt compliance
A

Factors for overall prognosis

77
Q
  • Determined after overall prognosis & affected by it

* Mobility, pocket depth, bone loss, furcation involvement, & other local factors

A

Individual tooth prognosis

78
Q

What prognosis according to McGuire and Nunn Classification?
o25% CAL &/or class I furcation involvement
oAdequate remaining bone support
oAdequate possibilities to control etiologic factors
oAdequate pt cooperation
oNo systemic environmental factors or well controlled systemic factors

A

Good prognosis

79
Q

What prognosis according to McGuire and Nunn classfication?
o25-50% CAL
oGrade I or easily accessible Grade II furcation involvement
oAdequate maintenance possible
oFew systemic complications

A

Fair prognosis

80
Q

What prognosis according to McGuire and Nunn classification?
o> 50% CAL
oClass 2 mobility
oInaccessible grade II furcation involvement; Grade III furcation
oDifficult to maintain areas &/or doubtful pt compliance
oPresence of systemic/environmental factors

A

-Poor prognosis

81
Q

What prognosis according to McGuire and Nunn classification?
o > 75% CAL
oTooth mobility > 2
oGrade II & III furcation involvements
oDifficult to maintain areas &/or doubtful pt compliance
oRoot proximity

A

hopeless prognosis

82
Q

What age of patients have a better prognosis?

A

older pts

younger pts show faster progression

83
Q

oSlight-moderate periodontitis → fair/poor prognosis
Upgrade to good prognosis if quit ____
oSevere periodontitis → poor/hopeless
Upgrade to fair prognosis if quit____

A

Effect of smoking on prognosis

84
Q

oWell controlled diabetics with slight/moderate periodontitis

A

good prognosis

85
Q 
oNeuro diseases (ie. Parkinson’s) that limit pts oral hygiene affects prognosis
Electric toothbrush may be helpful
A

cool story

86
Q

oPrognosis ____ for teeth with short-tapered roots & large crowns
Low CR ratio; more susceptible to occlusal trauma
oCervical enamel projections (enamel pearls, etc)
oRoot concavities
Pronounced on max. 1rst PM & MB root of max. 1rst molar
Increase SA for attachment, but difficult to clean

A

poor prognosis

87
Q

What is the prognosis for Chronic periodontitis (slight-moderate)?

A

good if inflammation is controlled

88
Q

What is the prognosis for Aggressive periodontitis ?

A

poor prognosis for involved teeth

89
Q

What is the prognosis for Periodontitis as manifestation of systemic disease?

A

fair/poor prognosis

90
Q

What is the prognosis for Plaque induced gingivitis modified by systemic disease?

A

prognosis depend on control of plaque and disease

91
Q

Good prognosis
oPrimary predisposing factor plaque
oTissue destruction is not reversible & poor control of 2° factors may make pts susceptible to recurrence of disease
Repeated episodes of ___ → prognosis downgraded to fair

A

NUG

92
Q

oOften immunocompromised

oPrognosis dependent on reducing local factors & managing systemic condition

A

NUP

93
Q

temporary restoration to remove plaque retaining factors

A

etiotropic phase

94
Q

trauma from occlusion; systemic diseases

A

widened PDL space

Perio Final (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions