Host responses to oral biofilms Flashcards

1
Q

How is periodontitis different to different health conditions?

A

Bacterial load is located generally “outside” the body making it a challenge for immune-inflammatory response to take action.

Plaque is a biofilm

Periodontitis is a result of dysbiosis of the normal microbiome

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2
Q

Where are biofilms located in periodontitis and gingivitis?

A

In gingivitis: Supragingivally

In periodontitis: Subgingivally

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3
Q

What risk factors tip the homeostasis towards dysbiosis? What factors favour resistance?

A

Resistance: Innate and adaptive immune response, inflammation, and other structural components.

Risk factors: Environmental factors such as smoking, dental plaque accumulation, socioeconomic status as well as host-specific factors such as genetic factors and overall inflammatory burden.

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4
Q

How does the epithelium provide a barrier to entry of microorganisms?

A

It forms a physical and biological barrier:

Physical barrier via turnover + peeling

Biological barrier via defensins, IL-8, adesion mols, and PMNs

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5
Q

How does GCF protect against inflammation?

A

Consists of plasma derived substances such as antibodies, cytokines and enzymes. Also composed of epithelium and immune cells.

GCF volume and flow increase with increasing inflammation.

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6
Q

What are the first defense cells against periodontitis?

A

Neutrophils

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7
Q

What innate immune system structures are protective?

A

Saliva: Prevents drying of gingiva and teeth with antimicrobial effects.

Epithelium: Physical barrier, inflammatory response via keratinocytes, and immune response via langerhans’ cells

Inflammatory response: Fluid component (GCF) and cellular components such as neutrophils and macrophages

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8
Q

What adaptive immune system structures are protective?

A

Humoral response

Cell-mediated response

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9
Q

What does LPS do to periodontium?

A

It stimulates macrophages to produce MMPs, IL-1b, and TNF-a

It stimulates fibroblasts to produce more MMPs

It stimulates IL-1b production as well as TNF-a by B cells and macrophages.

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10
Q

What are the histopathological classifications of clinical presentation of gingivitis?

A

Pristine: Histological perfection

Initial: Clinically healthy gingiva

Early: Early gingivitis

Established: Chronic or established gingivitis

Advanced: Periodontitis

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11
Q

What are the features of pristine gingiva?

A

Super healthy gingiva with no infiltrate

No bleeding

Pink, firm, scalloped outline, stippled and knife edge margin

Shallow gingival sulcus up to 3mm deep

Free of histological inflammation is extremely rare

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12
Q

What are the features of clinically healthy (not pristine) gingiva?

A

Healthy with infiltrate

Neutrophils and macrophages in JE

Lymphocytes in connective tissue

Collagen reduction not detectable clinically

Increase in vascular structures

Exudate and transudative fluid from vessels to tissues (GCF)

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13
Q

What does the initial lesion look like in periodontitis?

A

Change in microvascular plexus JE (vessels remain dilated and increase in number)

Arteriolas capillaries, and venules dilation

Hydrostatic pressure increase

Increased permeability

Exudate of fluids and proteins

Increased GCF

Enhanced PMNs migration

PMNs accumulate in JE and sulcus

VERY FEW PLASMA CELLS

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14
Q

What are the commonly seen features of ginigvitis?

A

10 to 20 days of plaque accumulation

Clinical signs of gingivitis

Redness, swelling, Blood on probing

Reversible after plaque removal

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15
Q

When does the early lesion from gingivitis form?

A

One week after plaque accumulation

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16
Q

What are the histological features of gingivitis?

A

Connective Tissue infiltrate 15% of volume

Fibroblasts degenerate

Collagen destruction

Clinically detectable inflammation

Proliferation of basal and JE cells

Coronoal rete ridges

17
Q

What are the features of an established lesion?

A

Increased fluid and leukocyte migration

More edematous swelling clinically

Plasma cells 10% on coronal connective tissue

Collagen loss in apical and lateral directions

Inflammatory cell infiltrate expands

Extension of rete pegs into connective tissue

JE detatched from tooth structure

Pocket epithelium with heavy cell infiltrate PMNs

Permeable and ulcerated pocket epithelium

18
Q

What are the clinical features of advanced periodontitis?

A

Pocket gets deeper

Apical plaque growth

Lateral and apical extension of infiltrate

Alveolar bone loss starts

Extensive fiber damage

Apical migration of JE from CEJ

Plasma cells predominate

19
Q

What is the function of antibodies?

A

Neutralization directly of antigens

Opsonization for Fc receptor-mediated phagocytosis

And complement activation

20
Q

What does complement activation do?

A

Leads to bacterial lysis

Inflammation

Phagocytosis of C3b-coated bacteria

21
Q

What do CD4+ helper T cells do?

A

Release various cytokines which lead to antibody response

Activate macrophages via IFN-gamma

Activate inflammation via TNF

22
Q

How does the humoral response provide protection against the bacteria from dental plaque?

A
  1. Plaque antigens diffuse through the JE
  2. Langerhan cells within epithelium capture and process the antigens
  3. APCs leave gingiva in lymphatics
  4. APCs go to lymph node and begin to stimulate lymphocytes to produce a specific immune response
  5. Antibodies are produced specific to the microbe
  6. Antibodies leave the circulation and are carried to the crevice in the transudate from the inflamed and dilated blood vessels
  7. Antibody action on microbes in the crevice can result in killing, aggravation, precipitation, detoxification, opsonization, and phagocytosis of bacteria
23
Q

How does cell mediated immunity protect in periodontitis?

A

Antigen penetration of JE contact to connective tissue

T-helper cells proliferate and release cytokines which activate other cells such as macrphages, B cells or T cells to stimulate, inhibit or kill.

T-helper cells on reexposure proliferate and produce cytokines.

24
Q

What do immune mediators do in periodontitis?

A

Cytokines induced by host response play a critical role in periodontal tissue breakdown.

Periodontal bone loss due to bacteria, high levels of cytokines, prostaglandins, MMPs, RANKL and low levels of IL-10 TGF-B, TIMPs and OPG

IL-6 and IL-8 are high inperiodontitis patients.

25
Q

What does IL-1 do in periodontitis?

A

Stimulates proresorptive cytokines, RANKL and TNF-alpha

26
Q

What does TNF-alpha do?

A

TNF-alpha accelerates bone destruction

27
Q

What does osteoclast activation result in?

A

RANKL and OPG stimulate osteoclasto-genesis and one resorption

If the RANKL/OPG ratio is high then it is proresorptive

If the RANKL/OPG ratio is low then it is antiresorptive

IFNgamma and IL-17 increase RANKL

IL-4 and IL-10 reduce RANKL/OPG ratio

28
Q

Which lymphocytes are antiresorptive?

A

TH2 and Tregs and antiresorptive

29
Q

Which lymphocytes are proresorptive?

A

Lymphocyte subsets TH1 and TH17 are proresorptive