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Perio > All Qs > Flashcards

All Qs Flashcards

1
Q

Patient motivation - how to encourage a patient

A

Motivation stemming from patient but support from dentist

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2
Q

What are TIPPS

A

TALK - Patient education and motivation (barriers and facilitators to care)
INSTRUCT - the patient into how to perform effective plaque removal
PRACTICE - in the surgery(ID brush) prior to going home
PLAN - how this can fit into daily life
SUPPORT - susequent appointments

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3
Q

OH advice

How to advise

A 
Clean 2x daily - at least 30 s per quadrant
Manual or electric toothbrush
Fluoride toothpaste (1450ppm)
Use modicied base technique
Interdental cleaning at least once daily

Tell show do approach

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4
Q

Aspects of NSPT

A

regular OHI reinforcement
regular NS instrumentation - supra/subgingival
smoking cesssation
dietary advice
Root surface debridement of >4mm pockets with subgingival deposits

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5
Q

Goal of NSPT

A

Reduced BOP <10%
Reduced pocket depth <4mm
Reduced plaque scores <15%

Stabilisation NOT cure of disease
Emphasise patient’s role in their own care

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6
Q

Warnings to patient prior to scaling/RSD

A

Sensitivity
gingival recession
LA - Bite cheek/lip/tongue

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7
Q

Why is it not advised to redebride a pocket in a followiing appointment if not finished

A

This is because initial healing, after the gross deposits have been removed, can make re-accessing the pocket more difficult and partial removal of deposits leaves behind rough areas which are ideal for bacterial
proliferation. It is advised that the clinician concentrates on as many teeth, sextants or quadrants as can be thoroughly instrumented in the time available.

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8
Q

Why would a patient be prescribed systemic antibiotics

A

In adjunct to RSD to supress bacterial species, ONLY in cases where patient will benefit from them.
Aggressive perio

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9
Q

How does a perio pocket repair

A

• Fibrin clot adheres to the root surface
• Progenitor cells from surrounding tissue proliferate,
migrate and differentiate
• Formation of bone, PDL and cementum

(Fibrin clot - fails to adhere to root surface, Downgrowth of epithelium between root and clot, Epithelial attachment to root)

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10
Q

Why do periodontal pockets fail to heal

A

Not full detoxification of root surface
Mechaniclal stress disrupts clot formation
LAck of space to accomodate regenerating tissue

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11
Q

Strategies for periodontal regeneration

A

Space maintenance and clot protection
• Selective cell repopulation
• Provision of progenitor cells
• Use of biological mediators

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12
Q

Indication for periodontal regeneration

A

ndications for Periodontal Regeneration

  1. Two and three-walled proximal defects
  2. Grade II mandibular furcation defects
  3. Grade II buccal maxillary furcation defects
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13
Q

Objective of bone grafts

A 
Space maintenance and clot protection
• Osteoconduction
Scaffold
• Osteoinduction
Promoting osteoblast activity
• Osteogenesis
Osteoblasts present in the graft
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14
Q

Types of bone grafts

A

Human - Allograft/Autograft
Xenograft - bovine/equine
synthetic - Polymer/hydroxyapatite/bioactive glass

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15
Q

Types of root resorption

A

Internal resorption
-inflammatory replacement

External resorption - pathological/physiological

  • External surface resorption
  • External inflammatory
    a) External apical resorption
    b) External periodontal (cervical) resorption
  • External replacement resorption
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16
Q

Aetiology of root resorption (2)

Detailed explanation

A

Trauma - injury/ortho/oral surgery
Stimulation - pulp/periapical infection

Injury -> Predentinumand odontoblasts (internal resorption) / Precementum (external)

Denuded mineralized tissue is colonized by odontoclast/ cementoclasts/dentinoclasts (tooth resorbing cells)

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17
Q

Internal resorption -
Initiated by
Aetiology

A

Initiated within pulp chamber/cana;
Aetiology - caries/trauma/fracture/idiopathic
- chronic pulpal inflammation / Bacterial extension into pulp
OCCURS WHEN PULP IS VITAL, dentine replaced by granulation tissue

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18
Q

Internal resorption - clinical presentation

Investigations and findings

A

Often asymptomatic, detect on Rg
Rg - Uniform round radiolucent area in canal (enlarged - like a snake digesting something)
Pulp tests - variable results
+ve - Apical pulp necrotic, coronal vital
-ve - Apical pulp vital, coronal necrotic
May progress to symptoms/increased mobility

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19
Q

Management of internal root resorption
Non perforated
Perforated

A

Non perforated - PULPECTOMY, remove granulation tissue (sodium hypochlorite and ultrasonic)

Perforated - PULPECTOMY, ns CaOH/MTA
XLA
Resection
Periodontal surgery - crown / ortho

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20
Q

External surface resorption aetiology

A

Post traumatic
masticatory forces (physiological)
self limiting - not detectable
Excessive ortho forces

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21
Q

External inflammatory resorption
Cause
Investigations and findings
Treatment

A 
NECROTIC PULP
-trauma (luxation/avulsion) / caries 
-ve sensibility tests
TTP
Mobility if extensive resorption

Rg - PDL space widens, loss of lamina dura, root surface irregular

Treatment - RCT,
CaOH placement as intracanal medicament 6-24mths
Periradicular surgery

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22
Q

Apical resorption - Rg features

A

Moth eaten appearance, canal anatomy unaltered

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23
Q

Orthodontic induced root resorption

A

Shortening/rounding of roots

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24
Q 
External cervical (priodontal) resorption
Origin
Aetiology
Clinical features
Rg
A

Originates in periodontium
trauma / ortho / periodontal disease / periodontal therapy
- Asymptomatic
-+ve sensibility tests

Clinically - Pink spot cervically (highly vascular granulation tissue)
Rg - moth eaten irregularity superimposed on RC

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25
Q

External Cervical resoption treatment

A
  1. No treatment - XLA as symptoms appear
  2. Immediate XLA
  3. Debridement and resorption - RCT if near pulp
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26
Q

External replacement resorption

  1. Aetiology
  2. Action
  3. Clinical features
  4. Rg features
A
  1. Luxation/avulsion - severe trauma, causes destuctionof cementum and root contact with bone - resorbed
    Ortho treatment
  2. tooth gradually replaced by bone
  3. Metallic percussion note, -ve sensibility tests, colour change, lack of physiological mobility, infraocclusion
  4. Lack of PDL space,
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27
Q

function of periodontium

A

Force dissipation / attachment to jaws

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28
Q

Horizontal forces source

A

Orthodontic forces

Intermittent

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29
Q

Response of healthy periodontal to occlusal forces

A

PDL width increased until forces dissipation of forces
Slight increase in tooth mobility
Successful adaptation - physiological
Demand eventually reduced - return to original width

Demand too much - continuing increase in PDL width, increase in mobility

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30
Q

Occlusal trauma - definition

Rg evidence

A

Tooth mobility that is gradually increasing
Symptoms
Rg evidence - Increased PDL width
In association with plaque induced inflammation

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31
Q

Occlusal trauma - associated with —— bone defect

A

VERTICAL
Plaque induced inflammation
Trauma induced inflammation

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32
Q

Significance of tooth mobility

Treatment
Spliniting reasons?

A

1.Progressive
Symptoms
Interrupting restorative treatment

  1. Controlled plaque induced inflam
    Correct occlusal relations

Splinting - mobility - adv LoA
Causing difficulty chewing
Need to be stabilised for debridement
LAST RESORT - OH difficulties

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33
Q

Deep traumatic overbite

-treatment

A

Treat plaque induced inflammation, relieve trauma - splint/ortho, restorative - occlusal stops

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34
Q

What is periodontal disease

A

A chronic inflammatory condition caused by anaerobic gram negative bacteria causing irreversible loss of attachment of teeth

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35
Q

Periodontal aetiology
Systemic/Local
Drugs - gingival hyperplasia

A

Systemic - Age/Race/Pregnancy(hormone imbalance)/puberty
Local poor OH/malpositioned teeth/crowded/calculus/iatrogenic - restorative margins/denture
Drugs - gingival hyperplasia
1. Cicclosporin
2. Phenytoin
3. ACE Inh

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36
Q
  1. How can pregnancy gingivitis occur.

2. Clinical features

A

1.Pregnancy can accentuate the response to plaque
2.Profuse bleeding
• Increased ease of bleeding
• Inflamed gingiva
• Bright red-bluish red colour gingiva
• oedematous interdental papilla
• Papilla may pit on pressure
• Smooth, shiny and soft (raspberry
like appearance)
• Marked vascularity
• Sometimes present with raspberry
like masses ‘pregnancy tumours

Not in healthy gingivae

37
Q

Pregnancy Gingivitis onset

A

2nd/3rd month
greater erythema and inflammation
greater bleeding tendency
Greatest severity between 2/3 trimester

38
Q

Histological features of pregnancy gingivitis

A

Non-specific vascularising, proliferative inflammation
• Marked inflammatory cell infiltration
• Oedema and degeneration of gingival epithelium and
CT
• Hyperplastic epithelium
• Accentuated rete pegs
• Reduced surface keratinisation
• Various degrees of intracellular and extracellular
oedema
• Leukocyte infiltration
• Copious newly formed engorged capillaries

39
Q

Pathophysiology of periodontitis in diabetic patients

A

Hyper-inflammatory trait
• Cytokines/Adipokines
• AGE/RAGE deposition in gingivae
• Microvascular changes in the periodontal tissues
• Deficiencies in the innate and adaptive immune
system
• Increased inflammatory bone destruction
• Reduced capacity for repair/remodelling
(RANKL/OPG)

40
Q

What is HbA1 and its significance in diabetes

A

Haemoglobin A1c - average blood glucose levels over a few months

41
Q

Prevention for diabetic patients

A

Achieve and maintain healthy body weight;
• Be physically active – at least 30 minutes of
regular, moderate-intensity activity on most
days. More activity is required for weight
control;
• Eat a healthy diet of between three and five
servings of fruit and vegetables a day and
reduce sugar and saturated fats intake;
• Avoid tobacco use – smoking increases the
risk of cardiovascular diseases

42
Q

Smokers and periodontal disease - Effect on periodontium

A

Long term chronic effect

Impair vasculature of periodontal tissues (masks the signs of gingivitis) -

43
Q

What are the features of aggressive periodontitis

A 
Neutrophil function defects
Root abnormalities
Hyper-responsive macrophage phenotype
LOW fetures of bacterial plaque
> proportion of A.A
44
Q

Localised Aggressive perio features

A

Localised
Pubertal onset
6’s and incisors
Robust antibody response

45
Q

Generalised aggressive perio features

A

Generalised (GAgP)
• Usually affecting subjects under 30 yrs but may
be older
• Generalised pattern AL affecting 3 teeth other
than 6s and incisors
• Clear episodic nature of destruction of
periodontal attachment and associated structures
• Poor serum antibody response to infecting agents

46
Q

Microbiology of aggressive perio

A

In relation to A.A - disease progression

High level of serum antibodies

47
Q

Microbiology of aggressive perio

A

In relation to A.A - disease progression
High level of serum antibodies
A.A virulence factor - leucotoxin/collagenase

48
Q

What are the virulence factors of A.A in Ag perio

A
  1. Leucotoxin - affects PNM function by suppressing chemotaxis
  2. Collagenases - breakdown of connective tissue and encourages loss of attachment
  3. Endotoxins - drives inflam response in gingival tissues
  4. fibroblast inh factor - prevent fibroblast attachment, affecting clot and attachment to root surface
  5. Soluble heat labile factor - inhibit groeth and proliferation of other microorganisms redcing competition
49
Q

Factors in Ag perio

A

Family history
Smoking
Papillion-Lefevre Syndrome

50
Q

What is Papillion Lefevre syndrome
Name some features

How is the oral cavity affected

A

Rare genetic disorder
Develop dryscaly patches of skin on palm of hands and soles of feet
(hyperkeratosis)

Oral cavity - teeth form and erupt normally but they exhibit chronic severe inflammation and degredation of periodontal tissues.

  • Gingivititis/stomatitis
  • Regional lymphadenopathy
  • greater pocketing
  • Halitosis and chewing painful
51
Q

Candidate genes for Ag Perio

A 
Cytokines e.g. IL-1, IL-10, TNF
• Receptors e.g. FMLP, Fc receptors
• Enzymes e.g. Cathepsin C
• HLA antigens e.g. HLADQ1
• Structural proteins Meng et al 2007
52
Q

what can a dentist - tell patient about Ag perio

-factors

A

Genetic
Poor OH
Smoking related
MUST monitor other family members

53
Q

How to treat patients with Ag perio

A 
Referral to specialist patient advised
Adjunct antibiotics with RSD
Plaque samples - lab
Encourage good OH
Full mouth debridement and CHX 0.2% mw
Systemic antibiotics -early in treatment
54
Q

Features of ANUG (Acute Necrotising Ulcerative Gingivitis)

A

-Blunt papillae
-Painful erythematous gingivae underneath
grey slough of necrotic mucosa/neutrophils
-Bleeding and halitosis
-Punched out crater like ulcers
-Necrosis of gingival tissue - eventually leads to PDL and bone

55
Q

Risk factors for ANUG

A 
Poor OH
Malnourished
Stress
Hormonal imbalance (Young adults)
Smoking 
Impaired immunity - HIV/Immunosuppressed
56
Q

What is necrotising stomatitis

A

Extension of necrosis beyond the mucogingival junction

Especially in those with HIV/Malnourished

57
Q

Pathology of ANUG

A

Fusobacterium
P intermedia
Treponema

58
Q

Treatment of ANUG and follow up

A

Gentle ultrasonic debridement
Improve OH
Smoking cessation
CHX/ Oxidising Mw

If systemic symps - 
Metronidazole 400mg (9 tablets) 1 tablet 3x daily for 3 days

Follow up - continuation of HPT and supportive therapy, tends to recur if all factors not addressed.
Can progress to NP

59
Q

What is a periodontal abscess,

How can they be caused

A

A localised excaccerbation of a pre existing perio (chronic) pocket.
Trauma or blockage of an existing pocket.

60
Q

What are the symptoms of a periodontal abscess

A 
Pain on biting
Swelling adjacent to tooth
Drainage to sinus
Discharge and halitosis
TTP
Tooth mobility
61
Q

Differential diagnosis for a periodontal abscess

A

Periapical abscess

Chronic perio - vital/non vital

62
Q

Treatment of a periodontal abscess

Follow up plan?

A

Incision and drainage
Gentle debridement of periodotal pocket
warm salt mw
XLA of teeth of poor prog

Antibiotics if systemic involvement
- metronidazole
Follow with HPT and supportive therapy

63
Q

Periodontal Surgery - when

Indications

A

Indications:
At re-eval 4-6 weeks after completion of NSPT.
Persistant pockets of >5mm
Good OH

Between re-eval and reconstruction
-If good plaque control but persistant deep pockets and BOP

64
Q

Treatment for patients with:

  • Poor OH and inflammation
  • Good OH and inflammation resolved
A
  1. Repeat HPT/cause related therapy

2. Supportive therapy and proceed with treatment plan

65
Q

Aims of periodontal surgery

A

Arrest disease process - complete RSD

Regenerate lost perio tissue

66
Q

Post op care of periodontal surgery

A 
CHX mw 0.2% for 1-2 weeks
Analgesia - 2-3 days
Antibiotics?
Remove sutures
Review and reappraise mechanical plaque control
67
Q

Healing process after open flap currettage

A

Formation of blood clot and organisation of collagenout tissue
Attachment of epithelium to root surface
Reduction in pocket depth - gaining of clinical attachment and gingival recession

68
Q

Types of bony defects

A

Infrabony - focal bone loss extends along root surface apically

  • ‘Three walled’ - buccal/lingual cortices preserved
  • ‘Two walled’ - buccal OR lingual cortex effaced
  • ‘single walled’ - both lingual/buccal cortices effaced

Intrabony

69
Q

Infrabony defect management

A

Closed/open RSD - healing by repair

Pocket elimination - osseous resection

70
Q

Perio surgery outcomes

A

NSPT/SPT show clinical improvement
reduced probing depths
SUpportive perio care needed for long term success

71
Q

How can periodontal therapy assist in restorative treatment

A 
Improves soft tissue management
Establishes stable gingival margin position 
Improves aesthetics
Reduced tooth mobility
Informs prognosis
72
Q

Issues with an inflamed gingival margin

A

Difficult moisture control
Poor aesthetics
Unstable margin position - subgingival crown margin

73
Q

Where should crown margins be ideally placed (measurements)

A

Within the gingival sulcus (0-0.5mm)
AVOID the biological width (2-3mm) - junctional ep(1mm) and Connective tissue (1mm)
Between crown margin and bone

74
Q

What are the issues with an overhanging restoration

A

Plaque retention, inflammation and bone loss

75
Q

What is ante’s law

A

The combined periodontal area of the abutment teeth should be equal to or greater than the periodontal area of the tooth or teeth to be

76
Q

What damage can be caused by FRP (crown/bridge)

A

Plaque retention
Poor location and fit of margins
Unfavourable transmission of occlusal forces
Pulpal damage

77
Q

What damage can be caused by RPDs

A

Plaque retention
Unfavourable transmission of occlusal forces
Direct trauma from components

78
Q

How can communication between the pulp and oral cavity/periodontal tissues occur

A 
Dentinal tubules
Iatrogenic damage - perforation
Lateral canals
Fractures
Resorption
Apical foramen
79
Q

Consequences when pulp becomes necrotic (periodontal tissues)

A

Direct inflammatory response from PDL at apical foramen

Leakage of necrotic tissue into periodontal tissues causing an inflammatory response

80
Q

Consequences to pulp if periodontal disease occurs

A

Pulp not usually directly affected until recession causes lateral canals to become exposed to oral cavity (not protected by sound cementum)

81
Q

How does a Primary Endodontic lesion with secondary periodontal involvement occur?
Treatment

A

-Suppurating endodontic disease left untreatment, leaks into periodontal tisseus
Plaque formed at gingival margin of sinus tract

-Both periodontal and endo treatment
Effective endo treatmetnt, perio determines the prognosis

82
Q

Primary periodontal lesion with secondary endodontic involvement

  • What gives a better prognosis
A

Apical progression of periodontal pocket, infection able to enter pulp via lateral canals/apical foramen - pulp becomes necrotic

  • Pulp vitality maintained by blood supply through apex
83
Q

What is a combined lesion

  • Features
  • Treatment
A

When coronally progressing endo lesion meets up with an apically progressing perio lesion

  • Tooth NON VITAL
  • periapical bone loss
  • Perio elsewhere in mouth
  • Large volume of attachment lost

-RCT- periapical healing
Periodontal therapy
Surgical exploration to confirm diagnosis

84
Q

Gingival recession symps

A

Poor aesthetics
Sensitivity
Tooth loss
Cervical lesions/root caries

85
Q

Recession treatment

A
  1. Monitoring and prevention
  2. Use of desensitizing agents, varnishes and dentine
    bonding agents
  3. Composite restoration
  4. Pink porcelain or composite
  5. Removable gingival veneers
  6. Orthodontics
  7. Surgery
86
Q

Recession aetiology

A 
Mechanical - vigorous toothbrushing
Tramatic occlusion
Trauma - lip piercing
Iatrogenic - poor crown margins
Teeth out of arch alignment
High frenal attachment
87
Q

what can be detected in a 6ppc (7)

A

pocket depth/gingival margin/tooth mobility/furcation involvement/BOP/LOA/

88
Q

idela HbA1c value

A

Ideal 48mmol/mol (6.5% or below)

89
Q

What occurs when a pulp becomes necrotic

-PDL response

A

When the pulp becomes necrotic, there is a direct inflammatory response by the periodontal ligament at the apical foramen and/or opening of accessory canals
• Inflammatory byproducts of pulpal origin may leach out through the apex, lateral and accessory canals and dentinal tubules to trigger an inflammatory vascular response in the periodontium.
• Among those are living pathogens such as bacteria and their toxic byproducts, fungi and viruses as well as nonliving pathogens
• Many of these are similar pathogens encountered in periodontal infections.

Perio (1 decks)

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