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BDS2; Integrated Clinical Practice > ICP L25: Aetiology and pathology of periodontal disease > Flashcards

ICP L25: Aetiology and pathology of periodontal disease Flashcards

1
Q

Clinical features of periodontal health

A

Gingivae =

  • Pink
  • Firm
  • Stippled
  • Knife-edged papillae
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2
Q

Clinical features of gingivitis

A
  1. Bleeding from gingivae
  2. Marginal redness
  3. Gingivae are swollen
  4. No bone loss/ attachment loss
  5. No mobility, recession or gaps
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3
Q

Clinical features of periodontitis

A
  1. Mobility and recession away from the CEJ
  2. Increased probing depths (pocket formation)
  3. Sensitivity due to root surface exposure (exposed dentine causes sensitivity)
  4. Drifting
  5. Gaps (black triangles)
  6. Bone loss on radiographs
  7. Long teeth
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4
Q

Why does periodontitis occur

A

Due to plaque maintenance and an inflammatory immune response - this is an irreversible process

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5
Q

What is the weakest point in the periodontal barrier

A

The junctional epithelium (especially during inflammation)

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6
Q

Describe the dysbiosis and key stone plaque hypotheses

A

Dysbiosis - the disruption on normal microbiome changes the symbiotic relationship between the host and microbes causing disease

Key stone - certain low-abundance microbial pathogens can orchestrate inflammatory disease by remodelling a normally benign microbiota into a dysbiotic one e.g. P.gingivalis

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7
Q

List three bacterial species present in periodontal health

A

Predominantly gram positive aerobic simple bacteria in symbiosis

  • S. Oralis
  • S. Mitis
  • S. Intermedius
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8
Q

List three bacterial species present in gingivitis

A

Predominantly gram positive/negative aerobic/anaerobic simple-complex biofilm in symbiosis/dysbiosis

  • A. actinomycetemcomitans
  • A. odontolyticus
  • Actinomyces species
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9
Q

List bacterial species present in periodontitis

A

Predominantly gram negative anaerobic complex biofilm in dysbiosis

  • Fusobacterium nucleatum
  • Prevotella intermedia
  • P. gingivalis
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10
Q

What is calculus

A

Calcified plaque which cannot be removed by brushing alone - it attaches to enamel, dentine and cementum and is covered by unmineralised bacterial plaque

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11
Q

What is supra gingival calculus

A

Creamy/Yellow calculus which is a precipitation of mental salts from saliva (Calcium phosphate/ HA)

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12
Q

What is sub gingival calculus

A

Brown calculus which is a precipitation of mineral salts from crevicular fluid (whitlockite) and is difficult to remove

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13
Q

What is an initial periodontal lesion

A

2-4 days after dental plaque accumulation with increased neutrophil migration and gingival crevicular flow

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14
Q

What is an early periodontal lesion

A

4-10 days after dental plaque accumulation becomes more excessive and there is increased neutrophils, monocytes, macrophages and lymphocytes with increased vascularity

There is collagen destruction to create space for the infiltrate and Rete peg proliferation (coronal part of JE)

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15
Q

What is an established periodontal lesion

A

2-3 weeks when neutrophils continue o migrate into tissues and gingival crevice and there is extensive sub gingival plaque

Plasma cells (B cells) predominate in the infiltrate and there is no loss of CT attachment or bone

This lesion can remain stable or can progress into a destructive lesion

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16
Q

What is an advanced periodontal lesion

A

Where there is gingival recession with fibrosis and inflammatory infiltrate in connective tissue and continued extension of sub gingival plaque

There is apical migration and ulceration of JE with periodontal ligament loss and alveolar bone resorption by osteoclasts

17
Q

What triggers the immune and inflammatory response in periodontitis

A

Bacterial products secreted: enzymes e.g. collagenase, protease, hyaluronidase

Bacterial membrane: LPS, lipoteichoic acid, capsular material

Metabolic products: butyric acid, propionic acid

18
Q

What are sentinel cells

A

Sensing cells = macrophages, dendritic cells, mast cells

These release alarm molecules (alarming) which are pro-inflammatory mediators

19
Q

How are pattern recognition receptors (PRRs) activated on sentinel cells

A
  1. PAMPs = Pathogen associated molecular patterns (on surface of pathogens)
  2. DAMPs = Damage associated molecular patterns (showing cell damage)
20
Q

What are the different alarming released by dentinal cells and what do they do

A
  1. Histamine - By mast cells : produce PGI2 dilating vessels and causing endothelial contraction
  2. Pro-inflammatory cytokines : TNF-a, IL-1B, IL-6, IL-8
  3. Prostaglandins : PGE2, PGI2
21
Q

How does type 1 inflammation occur

A

Activated by histamine (mins)

  • vasodilation and endothelial contraction = red and heat
  • inflammatory exudate moves into tissues = oedema
  • leukocyte extravasation : neutrophils from blood into gingival tissue
22
Q

How does type 2 inflammation occur

A

Activated by TNF-a and IL-1B (hrs)

  • more pronounced than type 1 activation
  • monocyte recruitment (macrophages in tissues)
23
Q

What is the function of neutrophils

A
  • Phagocytosis
  • Production of : chemokine, pro-inflammatory cytokines (IL-1b, TNF-a, IL-8), anti-inflammatory cytokines (IL-10), granule-derived antimicrobial molecules and enzymes (lysozyme), reactive oxygen species and matrix metallo proteases (enzymes breaking down tissues), substances aiding B cell survival, neutrophil extracellular traps
  • Expressing RANKL on surface and contribute to bone destruction
  • Regulate other immune cells T cells/DCs/NK cells/Macrophages
24
Q

What neutrophil defects are often associated with periodontitis

A
  1. Leukocyte adhesion deficiency (LAD) = deficient recruitment
  2. Lazy leukocyte syndrome = affects neutrophil function
  3. Neutropenia = low neutrophils
  4. Cyclic neutropenia = levels fluctuate from normal to low
  5. Produce XS pro-inflammatory cytokines
25
Q

What is the macrophage function

A

Antigen presenting cell
Phagocytosis
Produce pro-inflammatory cytokines (M1) and anti-inflammatory cytokines (M2)

26
Q

What is an acute phase response

A

When IL-6 is produced by dentinal cells and causes a systemic response which is increased by the liver complement proteins

27
Q

What is the complement system and what is its function

A

A cascade of circulating blood proteins activated by

  1. Classical (antigen-antibody complexes)
  2. Alternative (bacterial endotoxin, LPS on bacteria)
  3. Mannose binding lectin pathway

These cause

  • Opsonisation - sticking and marking antigen for phagocytosis
  • Cell lysis - rupturing bacterial cell wall
  • Chemotaxis - neutrophils and macrophages attract to antigen
  • Mast cell activation causing histamine release
28
Q

What is the role of T cells in periodontitis

A

Specific immune response where they promote/regulate inflammation and produce cytokines

  • T-helper cells : cytotoxic cells, mediating humoral immunity, mediating bone loss
  • T-regs : anti-inflammatory (IL-10)
29
Q

What is the role of B cells in periodontitis

A

Plasma cells produce antibodies and this predominates in established/advancing lesions

They express and produce RANKL which drives bone loss

30
Q

How is inflammation in gingivitis/periodontitis resolved

A
  1. Plaque removal
  2. Reversal of inflammation by reduction of pro-inflammatory mediators
  3. Resolvins = lipid mediators of inflammation
  4. Repair of connective tissue to produce new collagen forming new CT
31
Q

What is bone loss dependant on in periodontitis

A

RANKL-OPG pathway is the mechanism which regulates bone turnover and is dependant on a balance between

  1. Osteoblasts = bone forming cells and
  2. Osteoclasts = bone resorbing cells
32
Q

How does bone loss occur in periodontitis

A
  1. Receptor activator of nuclear factor kappa-B ligand RANKL is expressed by osteoblasts, and this is important in osteoclast formation, function and survival
  2. Receptor activator of nuclear factor kappa-B is located on osteoclast precursors and mature osteoclasts
  3. Osteoprotegerin (OPG) binds to RANKL and competitively inhibits RANKL expressed by the osteoblasts and other tissues (this is protective against bone loss)
  4. Oestrogen limits release of RANKL

BDS2; Integrated Clinical Practice (25 decks)

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