Ryan's Notes Flashcards by Tyler Brown

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

Necrotizing ulcerative gingivitis

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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

Necrotizing ulcerative periodontitis

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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

Etiology of NPD

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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

Histopathology of NPD

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Differential diagnosis of NPD

primary herpetic gingivostomatitis

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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)

Primary herpetic gingivostomatitis

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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

Gingival abscess

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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)

Periodontal abscess

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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)

Other reasons for periodontal related abscesses

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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)

Non-periodontitis related abscess

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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

Periodontal abscesses

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Differential diagnosis of periodontal abscess?

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

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Difference between periodontal abscess and endo abscess?

Periodontal abscess → tooth vital

* Endodontic lesion → tooth non-vital

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•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)

Anatomic connection between pulp and PDL

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

Primary endodontic lesion

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

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

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Tooth vital
Perio therapy → defect resolution
If lesion reaches apical foramen → effects pulp (pulp necrosis follows)

Primary periodontal lesion

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True combined lesion

•Independent pulpal & periodontal pathologies

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Effects of perio disease on the pulp

Perio disease (even severe) rarely leads to endo disease unless apical foramen involvement
Root surface defects, but no inflammatory changes in pulp

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•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)

Periodontal therapy effects on the pulp

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•Endo therapy complications → perforations & vertical fractures

Endo therapy effects on periodontium

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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

Acute phase reaction cascade

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•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

Characteristics of a risk factor

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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

Atherosclerotic vascular disease

AVD

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

Periodontal therapy effect on cardiovascular disease biomarkers

oImproved endothelial fxn & decreased intimal-medial thickness of arteries

Periodontal therapy effect on endothelial function

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

Strength of evidence for association between periodontal disease and AVD

• 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 ___

Association between periodontitis and adverse pregnancy outcomes

•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

Association between periodontitis and diabetes

•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

Association between periodontitis and risk of bacterial pneumonia

Odds ratio for what risk factor? | 2.5-3.7

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

Odds ratio for what risk factor? | 2.8-3.4

diabetes 2.8-3.4x more likely to have periodontitis

* Microbiota → necessary, but not sufficient to cause disease * Inflammation → necessary, but not sufficient to cause disease * HIV/AIDS * Osteoporosis * Obesity

Risk indicators for periodontitis

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

Risk predictors for periodontal disease

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

Prognostic factors for periodontal disease

variable contributing to cause of disease

etiologic factor

variable associatied with increased chance of developing disease

risk assessment

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

scleroderma

not an indicator of disease progression | oIndicates acute infection in pocket (possibly abscess)

suppuration

when probe depth reaches or passes mucogingival jxn | oSulcus depth at or apical to mucogingival jxn

Mucogingival defect

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

Furcation involvement

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)

Mobility

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

Different types of bone loss

Which bone loss defect is the best to regenerate?

-3 walled defect

Which bone loss defect is a lost cause?

1 walled defect

What is another name for a 2 walled defect?

crater

•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

Clinical definition of health

< 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

Gingivitis

< 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

Periodontitis

``` •Pain control •Reduction & 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 & esthetics - must meet pt expectations •Control of risk factors oProper plaque control oSmoking cessation oProper control of diabetes ```

Treatment goals

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)

Initial (hygienic) phase - etiotropic

What phase of treatment? | oPerio surgery; implant surgery

Corrective phase

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

maintenance phase - 3 month recall

• 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

Osseointegration = rigid fixation

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)

methods to increase osseointegration

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)

Background factors important for reliable osseointegration

* 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)

Initial implant stability - press fit implant placement

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

Steps used in surgical procedure

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

goal of surgical trauma- initiation of wound healing

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

24 hrs

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

1 week

What stage of bone healing? | new bone formation can be detected at ‘furcation sites’ of implant surface

2 weeks

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

up to 6 weeks

* 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)

Jumping distance concept

* 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

good time for implant loading

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

type of bone good for implants

Where is the ideal implant localization?

at cingulum

•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)

Requirements for implant

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

adjacent implant structures

What technique of implant placement? | submerged

2-stage implant placement

What technique of implant placement? | non-submerged

1-stage implant placement

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

microgap

* 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

clinical parameters used to evaluate peri-implant health

* Peri-implant probing * Existence of mobility * Radiographic examination

3 techniques to evaluate dental implants

What type of tissue to have around the implant?

Keratinized tissue/attached gingiva

* Age * Severity of disease * Systemic factors/smoking * Plaque/calculus & other local factors * Pt compliance

Factors for overall prognosis

* Determined after overall prognosis & affected by it | * Mobility, pocket depth, bone loss, furcation involvement, & other local factors

Individual tooth prognosis

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

Good prognosis

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

Fair prognosis

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

-Poor prognosis

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

hopeless prognosis

What age of patients have a better prognosis?

older pts | younger pts show faster progression

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

Effect of smoking on prognosis

oWell controlled diabetics with slight/moderate periodontitis

good prognosis

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

cool story

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

poor prognosis

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

good if inflammation is controlled

What is the prognosis for Aggressive periodontitis ?

poor prognosis for involved teeth

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

fair/poor prognosis

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

prognosis depend on control of plaque and disease

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

NUG

oOften immunocompromised | oPrognosis dependent on reducing local factors & managing systemic condition

NUP

temporary restoration to remove plaque retaining factors

etiotropic phase

trauma from occlusion; systemic diseases

widened PDL space

Ryan's Notes Flashcards

(94 cards)