L60: Aetiology and Pathogenesis Flashcards

1
Q

L60: In the traffic light system, what are the main changes happening between green (health) and orange (gingivitis)?

A
  • Change from symbiosis to dysbiosis of the biofilm;
  • Low biomass to high biomass;
  • Acute resolution of inflammation becomes chronic (persisting over time).
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2
Q

L60: In the traffic light system, what are the main changes happening between orange (gingivitis) and red (periodontitis)?

A
  • Further dysbiosis of the biofilm;
  • Disproportionate host immune response, hyper-inflammatory;
  • Failed resolution of inflammation;
  • Connective tissue and bone damage.
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3
Q

L60: What are some local plaque retention features for contributing to the trigger of gingivitis?

A
  • Calculus;
  • Restoration margins;
  • Crowding;
  • Mouth breathing.
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4
Q

L60: What are the main systemic modifying factors that influence the host’s response to plaque accumulation?

A
  • Sex hormones;

- Medication.

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5
Q

L60: Does plaque accumulation always cause gingivitis?

A

No, this can sometimes pass as gingival inflammation but without progression to gingivitis

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6
Q

L60: What are the signs of gingival health?

A
  • Well defined gingival margin;
  • Stippling (not always);
  • Pale pink (however colour also depends on race and lifestyle habits);
  • No BOP.
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7
Q

L60: In health, what makes epithelial barriers hard for bacteria to invade?

A

Rapid cell turnover therefore continuously shedding

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8
Q

L60: Provide details of the immune response occurring at sulcular epithelial barriers, during health.

A
  • Cellular level;
  • Small, controlled response;
  • Immune cells in GCF;
  • Inc. antibodies, lymphocytes, neutrophils
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9
Q

L60: What is GCF?

A
  • Gingival crevicular fluid;

- Inflammatory exudate from periodontal tissues.

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10
Q

L60: What are the signs of gingivitis?

A
  • Inflamed;
  • Loss of stippling;
  • Shiny, red appearance.
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11
Q

L60: Microbially, what happens to cause gingivitis?

A

Altered microbial colonisation of the biofilm, with increased biomass

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12
Q

L60: What happens to the immune response with gingivitis?

A
  • Increased immune response;
  • Increased flow of GCF;
  • Influx of immune cells (lymphocytes, monocytes, neutrophils);
  • Infiltration of plasma cells;
  • Proliferation and ulceration of the epithelium.
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13
Q

L60: Why do gingiva BOP with gingivitis?

A

Holey, instead of continuous but also inflamed and increased blood supply

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14
Q

L60: In terms of immune cells, what are more dominant with periodontitis, compared to gingivitis (and health)?

A

Plasma cells (B cells that produce antibodies)

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15
Q

L60: Besides a changed immune response, what other tissue changes occur with gingivitis and subsequently periodontitis?

A
  • Dilated vessels;
  • Vascular proliferation;
  • Collagen loss;

These progress further from gingivitis to periodontitis.

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16
Q

L60: What is the main clinical difference between gingivitis and periodontitis?

A
  • Irreversible loss of attachment (LOA);
  • Increase of pocket depth;
  • Apical migration of the junctional epithelium.
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17
Q

L60: What is a false pocket?

A

‘Pocket’ formation due to proliferation (+ inflammation) of the gingiva, no loss of epithelial attachment

18
Q

L60: For a true pocket, there must be…

A

Loss of attachment (junctional epithelium to tooth)

19
Q

L60: What lifestyle habit can often hide signs of pocketing before probing?

A

Smoking, due to vasoconstriction

20
Q

L60: Once periodontitis is triggered, what is the typical range of LOA per year

A

0.05- 0.1 mm per year, but can be worse (2mm). Can be continuous or episodic.

21
Q

L60: What are the properties of biofilms in health?

A
  • Protection against colonising species from competing organisms/ environment;
  • Facilitate uptake of nutrients;
  • Removal of metabolic products;
  • Maintaining appropriate physiochemical environment;
  • Bacterial communication.
22
Q

L60: What are the three bacteria commonly associated with periodontitis?

A

P. gingivalis, B. forsythias, T. denticola

23
Q

L60: What are the two theories of the common bacteria found with periodontitis?

A

Causation or Association

24
Q

L60: Describe two different mechanisms for how neutrophils attack pathogens.

A
  • Generation of reactive oxygen species, kill bacteria but can also cause bystander damage to host;
  • Release traps to trap bacteria and release mediators.
25
Q

L60: Alongside cytokines, what other mediators control inflammation/ bone resorption?

A
  • MMPs;
  • TNFa;
  • Prostaglandins;
  • Interleukins.
26
Q

L60: In terms of immune cells, how does the dominance of these change over the progression of periodontitis?

A
  • Initial lesion: mainly T-lymphocytes;
  • B cells and plasma cells at a later stage;
  • Locally produced antibodies (but can also be seen in the blood).
27
Q

L60: What are the protective functions of antibodies?

A
  • Inhibition of adhesion/ invasion;
  • Complement activation;
  • Neutralisation of toxins;
  • Opsonisation and phagocytosis.
28
Q

L60: Why do gums recede with periodontitis?

A

Protective function - to prevent biofilm entering circulation and having systemic impacts

29
Q

L60: What are MMPs and what are they responsible for in periodontitis?

A
  • Matrix metalloproteinases, a family of zinc and calcium dependent proteolytic enzymes;
  • Include collagenases;
  • Degrade connective tissue matrix.
30
Q

L60: What is the normal bone level, measurement away from ACJ?

A

1-2 mm

31
Q

L60: What are the two types of bone loss?

A

Horizontal and vertical (angular)

32
Q

L60: Which type of bone loss is usually easier to treat and why?

A

Vertical (angular) bone loss as there is already bone on one side of the tooth, regenerative material can be packed into the other side

33
Q

L60: How does vertical (angular) bone loss arise?

A

Immune response and tissue destruction in one area around a tooth, 2mm from tooth

34
Q

L60: What is horizontal bone loss?

A

Immune response and tissue destruction that encompasses the whole tooth surrounding

35
Q

L60: What are the risk factors for periodontitis?

A
  • Smoking;
  • Diabetes;
  • Stress;
  • Drugs;
  • Systemic disease;
  • Nutrition.
36
Q

L60: What are the risk determinants for periodontitis?

A
  • Genetics (male);
  • Gender;
  • Socioeconomic factors.
37
Q

L60: How does diabetes increase your risk of periodontal disease?

A
  • Can reduce blood supply to teeth and gums;
  • High blood sugar can also cause dry mouth, making gum disease worse;
  • Prone to oral infections (immunocompromised).
38
Q

L60: How does smoking increase your risk of periodontal disease?

A
  • Effects function of immune system (for the worse);
  • Depressed numbers of lymphocytes;
  • Increased production of inflammatory markers;
  • Change in bacteria (for the worse);
  • Vasoconstriction to oral tissues;
  • Impaired antibody production.
39
Q

L60: What other illnesses are periodontal disease often linked to?

A
  • Alzheimer’s;
  • Rheumatoid arthritis;
  • Poor pregnancy outcomes.
40
Q

L60: Remember, plaque is x but not y?

A
  • x: necessary;

- y : sufficient.