Periradicular pathology Flashcards

1
Q

What is the purpose of periapical pathology?

A

Part of host defence mechanism

Confines bacteria to root canals and prevents spread

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2
Q

What is the cause of endodontic disease?

A

Bacteria

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3
Q

Which microbes cause endodontic disease?

A

Mostly anaerobes (9:1 anaerobes to aerobes)

Porphyromonas and prevotella (bacteroides)

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4
Q

Which bacteria is strongly implicated in cases of sinus tracts and strong odours?

A

Prevotella melaninogenica

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5
Q

Which bacteria are present in extra radicular cluster formations?

A

Actinomyces israeli, propionibacterium propionicum

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6
Q

Where are the microbes?

A

In almost all infections, microbes stay in the root canal

The exception is acute apical abscess

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7
Q

What mostly passes apically?

A

Endotoxins

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8
Q

How do microbes get in?

A

Pulpal exposure, dentinal tubules, PDL, anachoresis

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9
Q

What are the different ways pulp can be exposed?

A

Trauma, vertical root fracture, pulp exposures during treatment, caries

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10
Q

What is anachoresis?

A

Positive attraction of blood borne microorganisms to inflamed or necrotic tissue during bacteraemia

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11
Q

What are perio/endo lesions?

A

Due to the communications between the pulpal and periodontal tissues

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12
Q

What type of inflammation has evolved to discriminate pathogens from self?

A

Acute

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13
Q

In acute inflammation, which cell is the first to react?

A

Neutrophils

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14
Q

How is inflammation achieved in acute inflammation?

A

TLRs act on immune cells and non-immune cells to recognise pathogen associated molecular patterns (PAMPs) on the bacteria

PAMPs bind to TLR-4 to increase inflammatory mediators

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15
Q

What are the three enzymatic systems involved in acute inflammation?

A

Kinin system, fibrinolytic system, complement system

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16
Q

When does chronic inflammation occur?

A
  • After acute inflammatory response doesn’t resolve
  • Without prior acute response where immune system responds to antigen
  • Infectious agent of low toxicity
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17
Q

What characterises chronic inflammation?

A

Infiltration of injured tissues by leukocytes and proliferative responses

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18
Q

Which lymphocytes are mostly involved in chronic inflammation?

A

CD4+ T lymphocytes

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19
Q

What type of lymphocytes are the majority of circulating lymphocytes?

20
Q

What are the two types of T cells?

A

CD4 (t helper) and CD8 (cytotoxic/suppressor)

21
Q

What are the subdivisions of CD4 cells?

A

T helper 1, T helper 2

22
Q

What do Th1 cells do?

A

Produce IL2, interferon and activates macrophages

23
Q

What do Th2 cells do?

A

Produce interleukins and regulate production of antibodies from plasma cells

24
Q

How are macrophages activated?

A

Activated CD4 cells make interferon which primes macrophages

Primed macrophages are activated by bacterial endotoxin and other mediators

25
Q

How do activated macrophages differ from non-activated (naïve) macrophages?

A

Larger, increased chemotaxis, ability to adhere, greater ability to phagocytosis and kill microorganisms, produce bone resorptive mediators

26
Q

Consequences of chronic inflammation?

A

Damaged tissue is replaced by fibrous CT, intermittent destruction of normal tissue and healing leads to scar formation

27
Q

What factors contribute to chronic inflammation?

A

Inadequate drainage, mobility (e.g., in bony fractures), presence of necrotic tissue acts as an irritant, mechanical irritation

28
Q

What three things do you need for peri radicular pathology?

A

Bacteria, pathway to pulp, time

29
Q

What is apical periodontitis?

A

Inflammation in the periodontal tissues around apex of tooth

30
Q

Functions of apical periodontitis?

A

Defence - confines bacteria, prevents spread into adjacent bone spaces, bone resorption

31
Q

What are the three different histological presentations of apical periodontitis?

A

Granuloma, abscess, cyst

32
Q

How to distinguish between a granuloma, abscess and a cyst?

A

Cannot distinguish clinically or radiographically (only histologically) except if there is a sinus tract then it is an abscess

33
Q

What is the most common histology of apical periodontitis?

34
Q

What is a granuloma?

A

Inflammatory lesion - lymphocytes, macrophages, plasma, fibroblasts, CT

Can be seen on tooth sometimes when extracted

35
Q

What happens histologically during abscess formation?

A

Change in cellular dynamics - dramatic increase in phagocytic activity and number of PMNs

36
Q

What is a chronic abscess?

A

Persistent, walled off chronic inflammatory tissue keeps areas of suppuration localised

37
Q

What are cysts?

A

Epithelium lined cavities that contain fluid or semi-solid material

38
Q

Where do apical cysts originate from?

A

Epithelial cell rests of Malassez

39
Q

What are the variations in cyst linings?

A

Continuous, disrupted, missing

40
Q

What is a pocket/bay cyst?

A

Inflammatory cyst, sac-like, open to and continuous with the root canal space

41
Q

What is a true cyst?

A

Within the apical granuloma, no connection between cavity and root canal surface

42
Q

Where can cysts of upper teeth originate from?

A

Maxillary sinus

43
Q

What can we do with Endodontics?

A

Reduce bacterial levels to negligible, prevent endotoxins from reaching apical tissues, entomb/incarcerate any surviving bacteria, prevent ingress of fluid

This leads to the active lesion subsiding and bone regeneration

44
Q

What is the success rate of endodontic treatment in teeth without AP?

45
Q

What is the success rate for endodontic treatment in re-treatment cases without AP?

46
Q

What is the success rate of teeth with Apical periodontitis?

47
Q

What is the success rate for re-treatment cases with AP?