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CSP3 YR5- Restorative RESET > Periodontal Disease > Flashcards

Periodontal Disease Flashcards

1
Q

Inflammation? Definition?

A

The reaction of living tissue to injury or infection

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2
Q

Immunity? Definition?

A

The ability of an organism to
resist disease, through the activities of specialised blood cells or antibodies produced
by them in response to natural exposure or inoculation

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3
Q

Adaptive vs Innate? Differences?

A

Innate: No time lag, not antigen specific and no memory
Adaptive: Lag period, antigen specific and memory development

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4
Q

Innate immunity? Dental-related?

A

Saliva, Epithelium and Inflammatory response

Saliva: prevents drying, antimicrobial (IgA, peroxidase, lysozyme and lactoferrin)

Epithelium: physical, inflammatroy via keratinocytes and immune response via macrophages

Inflammatory response: GCF, neutrophils and macrophages

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5
Q

Saliva? Immunity characteristics?

A
  • Stimulate gut secretory immune system
  • Activated gut lympho migrate to sailavry gland and secrete IgA, influencing bacterial attachment and allowing them to be swallowed
  • Peroxidase kills bacteria
    lysozyme weakens +ve wall
  • Lactoferrin binds iron for bacterial growth
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6
Q

Oral Mucosal Surfaces? Immunity characteristics?

A 
IgA
Mucins
Saliva
Serum IgG
Langerhans' cells
Membrane coating
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7
Q

Epithelium? Immunity characteristics?

A

Physical
Inflamm response via Keratinocytes
Immune via Langerhans’

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8
Q

Junctional epithelium? Immunity characteristics?

A

High cell turnover
Neutophils found in JE migrate to sulcus (role in jost defence)
Cells maintained in early maturation, which in-turn does not form membrane coating granules, and so JE is permeable to some plaque

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9
Q

Inflammatory response? JE?

A

Cells in JE release IL-1/8, TNF-a and cytokine-induced neutrophil chemo-attractant-2

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10
Q

Immune response? JE

A

Langerhan’s cells

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11
Q

Features of inflammation?

A 
Pain
Swelling
Redness
Increased temperature
Loss of function
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12
Q

Cells of the immune system? Differentiation?

A

Stem cells form Lymphoid stem cells and myeloid progenitor cells
LSC - B cell, T cell and NK
B - Plasma and memory
T - helper and killer

MP - neutro, eosino, baso, mast and mono
Mono form dendritic and macrophages

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13
Q

Neutrophils? Function? Bacteria in plaque matrix vs unattached?

A

In plaque matrix:

  • neutrophil attach to plaque
  • secretes enzymes and H2O2
  • kills bacteria
  • plaque dissolved
  • washed away by GCF
  • damaged caused

Unattached:

  • neutrophils recog and bind bacteria, phago into vacuole
  • produces antibac granules and H2O2
  • digest bacteria
  • remnants expelled
  • damage caused
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14
Q

Macrophage? Function? Inflammation vs Immunity?

A

Inflammation:

  • phago dead and dying cells
  • modulate fluid and cellular components
  • secrete tissue-degrad zymes
  • secrete IL-1, TNF-a and prostagl

Immunity:

  • traps and presents antigen, while CD44 acts as anchor
  • secrete IL-1/TNF-a
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15
Q

Humoral response? Process?

A
  1. Langerhans’ cells take antigen to lymph nodes and present to lymphocytes – clonal expansion
  2. B-lymphocytes differentiate into plasma cells and secrete antibody against antigen
  3. Antibody thought to be protective – IgG, IgA
  4. Antibody produced systemically or locally.
    Aggregate micro-organisms, activate complement system to lyse bacteria, opsonisation + phagocytosis via neutrophils
  5. Antibody titres vary between individuals, and in response to treatment
  6. High levels indicate either positive immune response or an inability to eliminate pathogen
  7. Antibody avidity is a measure of effective immune function.
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16
Q

Local antibody production? JE? Process?

A
  1. Plaque antigen diffuses through JE
  2. Langerhans capture antigen in JE
  3. APC leave gingiva in lymphatics
  4. APC reach lymph node and stimulate specific immune response
  5. specific abs are produced by plasma cells within lymph node and travel back to gingiva via BVs
  6. Abs leave circulation and are carried to the crevice in the transudate
  7. Abs bind to antigen causing aggregation, precipitation, detox, opson and phago.
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17
Q

Cell mediated response? JE?

A

No Antibody involvement
1. Antigen processed and presented to T Cell
Receptor on T-helper cell (Th1, Th2)
2. T-helper lymphocytes produce cytokines to assist
B-cell differentiation into Plasma Cells, or activate
Neutrophils and Macrophages
3. T-helper 1 cells stimulate cytotoxic T Cells (Tc) –
Aggregatibacter Actinomycetemcomitans
Gingivitis – predominantly T cell response
Periodontitis – predominantly B Cell / Plasma Cell
response

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18
Q

Bone destruction? -ve vs +ve?

A

-ve:
- LPS
+ve:
- peptidoglycan

Walls have different effects on the communication of the cells
Act complement

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19
Q

5 stages of periodontitis development?

A 
Pristine gingiva
Initial lesion
Early lesion
Established lesion
Advanced Lesion
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20
Q

Pristine gingiva? Characteristics?

A

Free from histological inflammation, however this cannot be achieved due to the presence of bacteria

Classification of 2017 created clinical gingival health

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21
Q

Initial lesion? Characteristics?

A
  • Inflammation within 24 hours of plaque accumulation – Vasodilation, ↑ GCF
  • Neutrophils migrate into gingival sulcus (ICAM-1, ELAM-1)
  • A few lymphocytes / macrophages
  • Lymphocytes bind to connective tissue (CD44)
  • Cellular Response develops in 2-4 days
  • Plaque form on supragingiva
  • WBCs in JE
  • Increased vasc in CT

Under the new guidelines this is considered ‘Clinical Gingival Health’

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22
Q

Early lesion (1 week)? Characteristics?

A
  • Inflammatory infiltrate increases
  • Vessels dilated / More vessels
  • ↑ Lymphocytes + - —-Neutrophils
    • Very Few Plasma Cells
    • Fibroblasts show cell damage
  • Loss of Gingival Collagen
    Basal cells of Junctional +
    Sulcular epithelium proliferate (Mechanical Barrier)
    • Rete Peg Proliferation
    • Some Coronal Epithelium lost
    – plaque starts to extend
    subgingivally
    • Can Persist without
    progressing to Established
    Gingivitis
  • Plaque biofilm formation
  • Intact alveolar bone
  • CEJ still at JE
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23
Q

Established lesion? Characteristics?

A
  • ↑ GCF
  • ↑ Inflammatory infiltrate
  • Neutrophils predominate, ↑ Migration
  • Plasma Cells form 10-30% of infiltrate
  • Fibroblasts continue to show cell damage
  • Loss of Gingival Collagen
    Laterally and Apically
  • Rete Pegs extend further
  • Junctional epithelium no
    longer closely attached to
    tooth – “False Pocket”
  • Gingivae Red + Swollen
  • May remain stable or progress to Periodontitis (final stage)
  • Supragingival plaque extending subgingivally
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24
Q

Gingivitis classification?

A

Clinical Gingival Health: no attachment loss and less than 10% BOP

Localised Gingivitis: no attachement loss and between 10-30% BOP

Generalised Gingivitis: no attached loss and greater than 30% BOP

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25
Q

Advanced Lesion (Suprabony)(Periodontitis)? Characteristics?

A
  • Inflammatory infiltrate extends apically and laterally
  • Plasma cells predominate (>50% of cell types)
  • Loss of periodontal connective tissue attachment
  • Apical Migration of Junctional Epithelium – True pocket formation
  • Alveolar Bone Loss
  • Periodontitis (Stage 1)
    in this example as up
    to 10% bone loss
  • Loss of attachment 1-2mm
  • Pocket 4-5mm
  • Pocket epithelium (ulcerated and leaky)
  • Subgingival calculus covered by plaque
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26
Q

Advanced Lesion (Infrabony)(Periodontitis)? Characteristics?

A
  • Same as Suprabony but 10-33% bone loss (stage 2)

- Loss of attachment 3-4mm

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27
Q

Gingivitis to Periodontitis progression?

A
  • Regulated by variable expression of integrands and
    other adhesion molecules at the epithelial –
    connective tissue interface (ICAM-1, ELAM-1, CD44).

Matrix Metalloproteinases

Reactive Oxygen Species

Cytokines & Growth Factors
• Platelet Derived Growth Factor (PDGF)
• Insulin-like Growth Factor (IGF)
• Interleukin-1 (IL-1)
• Transforming Growth Factor β (TGF- β)
• Prostaglandin E2 (PGE2)
• Interferon γ (IFN- γ)
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28
Q

Matrix Metalloproteinases? Aid periodontitis progression process?

A
  • MMPs synth and secreted by inactive precursor, converted to active (activation by proteinases)
  • GF and cytokine reg MMP production (IL-1 and TGF-b)
  • serum and tissue inhibitors neutralise activity of MMP
  • TIMP prevet conversion of precursor of MMPs to active form
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29
Q

Asynchronous multiple burst theory? Clinical attachment loss (CAL)

A
  • Multiple active sites break down within a short time, with long periods of quiescence
  • Periods of activity may be clustered around phases of patient’s life (risk factors)
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30
Q

Periodontal tissue healing? Process? Overview?

A
  • Starts with acute inflammation (24-48hrs)
  • Dental treatment and maintenance leads to healing
  • Includes reduced:
    vasodilation, gingival crevicular fluid, inflamm cells and the pocket ulceration heals
  • Fibroblasts prolif forming collagen fibres and ground substance forming mature CT
  • Formation of long JE and bony remodelling
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31
Q

Bacterial flora? Characteristics during healing?

A
  • Reduction in total numbers
  • Shift from -ve anaerobes to -ve aerobes
  • From disease associated to health
  • Reduction in plaque bulk
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32
Q

1 week post-treatment from advanced lesion? Composition?

A
  • Reduction in number of neutrophils in gingival crevice
  • CT infiltrate reduces
  • Reduction in gingival swelling
  • Pocket ulceration healing
  • Fibroblast prolif
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33
Q

1 month post-treatment? Composition?

A
  • Gingival recession (shrinkage)
  • New fibrous tissue formed
  • Long JE attachment begins to form
  • Alveolar bone remodels (no regen)
34
Q

3 month post-treatment? Composition?

A
  • Gingival crevice (low neutrophil load)
  • JE re-establihsed at CEJ but longer
  • New gingival CT mature with minimal inflamm infiltrate
35
Q

Summary of tissue healing response?

A
  • Shrinkage of tissue leading to recession
  • Formation of long JE
  • Tightening of gingival cuff (as collagen fibres reform)
  • Small regain in attachment
36
Q

Regulation of healing? Characteristics?

A
  • Stim of TGFa
  • Reg of TGFb (repair)
  • Epithelial cell attachement promosted by base mem prots (Laminin)
  • Firoblast stim (PDGF)
  • Reg of MMPs
  • Matrix synth and prolif (fibtronectin and tenascin)
37
Q

Signs of failure post-treatment? Characteristics?

A
  • Bleeding on probing
  • Redness
  • Swelling
  • Deep pockets or increasing depths
  • Suppuration
  • Increasing mobility
38
Q

Bleeding on probing? Rules?

A
  • 20-30% of sites bleed on probing will go on to demonstrate further attachment loss
  • Bleeding from the base of the pocket suggests a site is not responding, especially if it persists
39
Q

Reasons for failure post-treatment?

A
  • Lack of compliance or dexterity
  • Residual subgingival calculus deposits harbouring subgingival plaque (deep pockets, furcations, concavities, grooves and inexperienced operator)
40
Q

Consultation Process? Basic Process?

A
  • History and examination
  • Diagnosis
  • Treatment Plan
41
Q

2017 periodontal classification? Codes and consequences?

A

Codes ranging from 0 to 4

  • Code 0/1/2: gingival health or at maximum generalised gingivitis
  • Code 3: depending on the pocket sizing >4mm continue to code 4 treatment and <4mm treat like code 0/1/2
  • Code 4: dental recession, pockets greater than >4mm, needs constant support, becoming periodontitis
42
Q

Treatment planning? Initial, corrective and supportive periodontal therapy?

A

Initial: cause-related
- related to disease, control infection and managing factors (provisional treatment plan)

Corrective therapy:
- patient’s oral hygiene has improved but the disease is still present, option of periodontal surgery

Supportive therapy:

  • prevent recurrence if disease
  • stabilises condition
43
Q

Initial therapy? Characteristics?

A

Systemic: risk factors;
- smoking, alcohol and diabetes

Oral hygiene:
- advice and support on self-performed plaque control (tooth brushing techniques and interdental brushing)

Local factors:
- removal/modification of local risk factors (calculus)

Provisional treatment plan:
- extractions (untreatable teeth), endodontics, occlusal adjustments and hypersensitivity

44
Q

Communication between you and the patient? Non-verbal and verbal skills?

A

Non-verbal:

  • dress and appearance (first impressions stick)
  • facial expression
  • eye contact (depending on patient)
  • proximity; personal space and intimate contact in oral cavity (privilege)
  • seating position; face to face and delivered at level height or lower

Verbal:

  • open questions (rapport)
  • focused questions (precision)
  • closed questions
  • clarification (re-interpretation of the patient’s response)
  • listening and empathy
45
Q

Communication barriers? Problems they may cause?

A
  • patient not in control (safe word)
  • telling off (non-judgmental)
  • embarrassment
  • peculiarity of encounter (respectful)
  • vulnerability lying (adjust to situation)
  • after effect of injection (calm them down, no important info post)
  • discomfort (inform for reduced shock)
  • expense (best to relieve pain)
  • the unknown (running commentary)
46
Q

Communication aids? how can they be useful?

A
  • pictures and diagrams (illustrate problem and teach)
  • x-rays (show problem)
  • disclose plaque (show)
  • show sites of disease and health comparison
  • show sites of problem
  • check patient understands

Video/pictures for patient reference in the future

47
Q

Key communication skills? Do’s and Dont’s

A

Do’s:

  • positivity
  • normal jargon
  • set attainable targets
  • give patients time
  • tailor info
  • expect relapse (but give support)
  • never give up

Dont’s:

  • telling off
  • blaming
  • overloading
  • jargon
  • take offense to patient failure
48
Q

Health belief model? What is it?

A

Gaining attention:
- inform patient has incurable disease

Perceived susceptibility:
- prevalence from statistics to highlight they are different

Perceived severity:
- personalised biofeedback by use of radiographs and plaque disclosure

Motivation to change:
- find a reason to motivate their change

Perceived barriers:

  • realistic with level of commitment
  • higher level of care needed compared to most

Perceived benefits:
- reduce bleeding, mobility ad loss
- improvements in health
(link to low birth weight babies, erectile dysfunction and CVD)

49
Q

Non-surgical periodontal therapy? Definition?

A

Directed at the removal of supragingival and
subgingival plaque and calculus deposits, plus
local plaque retention factors, and forms the
mainstay of periodontal management in
general dental practice

50
Q

Toothbrushing techniques? How, where, why and when?

A
  • twice a day
  • 2 mins
  • systematic
  • look in mirror
  • small head brush
  • on the gumline and tooth
  • angle bristle at 45
  • modified Bass technique
51
Q

Interdental cleaning? options?

A

65% of cleaning achieved by brushing

need interdental brushes, floss, powered devices and woodsticks

52
Q

Overview of periodontal surveillance? basic?

A
  • Initial therapy (cause-related)
  • Review (8-12 weeks)
  • Then either corrective therapy or maintenance therapy
53
Q

Initial therapy? Treating the cause?

A

Systemic phase: with GP

  • smoking cessation
  • diabetic control
  • stress management

Acute phase:
- emergency treatment

Cause related phase: restorative stabilisation

54
Q

Cause related therapy? What to do with the patient?

A
  • OHI/Motivation/RA
  • Setting goals (SMART)
  • Determine restorability
  • extract hopeless teeth
  • non surgical debridement
  • removal of plaque retentive factors
  • initial endodontic therapy
55
Q

Goals of treatment? Targets?

A
  • Reduction of Plaque Index (≤ 15%)
  • Reduction of Gingival Index (≤ 20%)
  • Reduction of Bleeding on Probing (≤ 20%)
  • Reduction of Pocket Depth (≤ 4mm)
  • Elimination / Reduction of Furcation Involvement
  • Absence of pain
  • Individually satisfy aesthetics and function
56
Q

What happens in a 8-12 week review?

A
  • Plaque Index (disclosed)
  • Gingival Bleeding Index
  • Pocket Probing Depths
  • Free Gingival Margin (Recession / Overgrowth)
  • (Clinical Attachment Loss)
  • Bleeding on Probing
  • Mobility
  • Furcations
  • Suppuration
57
Q

A brief risk assessment of the patient? to check what the patient may need from the future?

A
  • Presence of Bleeding on Probing
  • Prevalence of residual pockets > 4mm
  • Loss of teeth
  • Bone loss in relation to age
  • Systemic and Genetic conditions (diabetes,
    stress etc.)
  • Environmental factors (smoking)
58
Q

Corrective therapy? when the disease hasn’t cleared/improved

A

Resective/regenerative surgical procedures

Adjunctive local antimicrobial

Definitive prosthodontic restoration:

  • occlusal adjustments
  • endodontics
  • implants
  • orthodontics
59
Q

Maintenance Therapy? Periodontitis is a life-long disease?

A

Start with 3 month appointments to assess stability and change

Therapy:
- Periodic professional supportive care (initially 3
monthly, but dependent on risk assessment)
- Reinforcement of Oral Hygiene Instruction and
Motivation
- Comprehensive professional supra and
subgingival plaque removal (biofilm disruption)
- Re-instrument sites with Calculus, BOP +ve or Pockets ≥ 4mm
- Annual multi-pronged periodontal stability and
risk reassessment
- Radiographic updates and therapeutic
interventions as needed

60
Q

Dental hypersensitivity - why? how? causes?

A

Why:
- when the dentine is exposed (if cementum has been removed), exposed dentinal tubules
How:
- stimulus can move the fluid within the tubules that interact with the A delta fibres that cause sharp pain
- larger tubules, more fluid movement and more pain
Causes:
- dietary acids such as (fruit juice, carbonated drinks, alcohol, energy drinks, fruits, picked food and tomato ketchup)
- dietary alkalines such as dairy

61
Q

Dentinal hypersensitivity - symptoms?

A
  • Pain to thernal stimuli
  • Chemical stimuli (acid or alkali)
  • Mechanical stimuli (brushing and root instrumentation)
  • Pain is short-lived and sharp
  • Subsides when stimulus removed
62
Q

Dentinal hypersensitivity - advice?

A
  • non teeth whitening toothpaste
  • dietary advice
  • lifestyle
63
Q

Dentinal hypersensitivity - modes of treatment?

A

Dietary advice:
- minimise frequency of acid intake
Occlusion of exposed dentinal tubules:
- tooth sensitive toothpaste (strontium compounds, fluoride, insoluble calcium compounds and resins)
Depolarisation of pulpal nerve fibres (A-delta):
- potassium nitrate (active ingredient in sensodyne)

64
Q

Dentinal hypersensitivity treatment - modes of action?

A
  • Potassium nitrate diffuses up the dentinal tubules, but takes a few weeks to get to therapeutic dose
  • Compounds travel up the dentinal tubules to reduce the fluid movement in the tubules, stopping the stimulus to the Adelta fibres
65
Q

Dentinal hypersensitivity treatment - cascade of treatment?

A
  • dietary advice (spitting not rinsing)
  • toothpaste (various options, non-tooth whitening)
  • topically applied agents (duraphat or seal and protect)
  • restorations (over root), but this needs to be prepared
  • devitilisation and root canal treatment (possible extraction)
66
Q

4 levels of periodontal health? Levels?

A
  1. Pristine health - absence of inflamm
  2. Clinical health - minimal inflammation
  3. Periodontal stability in reduced periodontium
  4. Periodontal disease remission/control I’m a reduced periodontium
67
Q

Clinical gingival health on a reduced periodontium - stable - clinical signs? Successful treatment?

A

Clinical signs:
- absence of BOP, inflammation and symptoms
Differences to gingival health:
- reduced clinical attachment and bone levels
- not at CEJ and root exposure
Successful treatment: absence
- BOP
- inflammation
- symptoms
- adequate OH (highly variable)
- manageable pocket depths <4mm (border between stability and activity)

68
Q

Reduced periodontium (biofilm-induced) - how to keep stable?

A

Stability factors:

  • local and modifying factors (diet and glycaemic control)
  • minimising inflammation (oral hygiene)
  • stabilising attachment loss
69
Q

Plaque induced gingivitis on a reduced periodontium - treatment plan?

A

Treatment plan: high susceptibility

  • gingival on specific sites remain on periodontal maintenance and should be monitored closely
  • difficult to determinenthershold between gingivitis and react of periodontitis
  • BOP and PPD >3mm important but overall loss and proven susceptibility is more significant
70
Q

Periodontium - Stages of diagnosis - what to identify?

A
  • determine whether you have intact or reduce periodontium
  • deduce whether a BPE or full mouth exam is necessary
  • look for health or presence of disease
  • distribution across the oral cavity
  • severity and grading of periodontitis (if present)
  • risk factors: lifestyle, poor dexterity, OH, plaque retentive factors
  • overall status of periodontium (stable, unstable or in remission)
71
Q

Plaque biofilm-induced gingivitis - Clinical signs?

A

Clinical signs: inflammatory lesion from interactions between biofilm and host immune repsonse
- no loss of attachment, no subgingival involve and CEJ intact

72
Q

Appropriate times to use a BPE?

A
  • screening tool
  • guide clinicians to arrive at a provisional diagnosis
  • BPE guides for further diagnostic measures
  • if considered a periodontitis patient, go straight to full charting
73
Q

Reduced periodontium (non-periodontitis patient)

A
  • no bacteria involvement
  • recession or crown lengthening
  • caused by trauma
  • picking at gingiva
  • excessive brushing
    Need to be able to differentiate
74
Q

BPE code 0/1/2 - Clinical signs?

A

Periodontal assessment with a comprehensive history
No evidence if periodontitis, go ahead with BPE
Clinical signs: PI and GI
- 0 health BOP (<10%)
- 1 localised gingivitis (>10-30%)
- 2 generalised gingivitis (>30%)
Aided with PI and GI information

75
Q

Risk factors for gingivitis - local and systemic?

A

Local: encourage plaque accumulation at specific sites
- retention factors
- oral dryness (xerostomia)
Systemic: negatively influence the immune-inflamm repsonse to dental plaque
- smoking
- metabolic factors: diabetes
- nutritional factors: vit deficiency
- pharmacological agents
- sex steroid hormones: puberty/preganncy
- haematological conditions: cancers

76
Q

Periodontitis - inclusion for a diagnosis?

A
  • type and extent
  • peridontitis stage and grade
  • current periodontal status and risk factor profile
77
Q

Periodontitis - clinical signs? Overview? Critical sign

A

Overview:
- loss of CT attachment and alveolar bone
- preceded by plaque biofilm induced gingivitis
Clinical signs:
- loss of attachment, not at CEJ, loss of bone, loss of PDL
- no cure
- PD of >6mm
Critical sign:
- interdental clinical attachment loss is detectable in >2 non adjacent teeth
- or buccal CAL >3mm with >3mm PPds in more than 2 teeth not attributable to periodontitis related causes (gingival recession)

78
Q

Periodontitis - treatment/diagnosis

A

Full periodontal chart (UNC15):
- PPDs over 4mm, BOP, furcations and supparation
PI and GI
Radiographical evidence

79
Q

Periodontitis - diagnosis? Inclusion?

A
  • Type: periodontitis
  • Distribution: localised and generalised (molar incisor perio)
  • Stage: I-IV regarding to bone loss (I early, II moderate, III severe and IV very severe) (coronal mid and apical loss of bone, from radiograph)
  • Grading: A-C rate of bone loss (%s) (A slow, B moderate, C rapid) related to age
  • Status: stable/unstabel/remission
  • Risk factors: smoking
80
Q

Staging of periodontitis - with classification?

A

Stage I: - <15% or <2mm attachment loss of CEJ
Stage II: coronal third of root
Stage III: mid third of root
Stage IV: apical third of root

CSP3 YR5- Restorative RESET (44 decks)

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