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
How do activated macrophages differ from non-activated (naïve) macrophages?
Larger, increased chemotaxis, ability to adhere, greater ability to phagocytosis and kill microorganisms, produce bone resorptive mediators
26
Consequences of chronic inflammation?
Damaged tissue is replaced by fibrous CT, intermittent destruction of normal tissue and healing leads to scar formation
27
What factors contribute to chronic inflammation?
Inadequate drainage, mobility (e.g., in bony fractures), presence of necrotic tissue acts as an irritant, mechanical irritation
28
What three things do you need for peri radicular pathology?
Bacteria, pathway to pulp, time
29
What is apical periodontitis?
Inflammation in the periodontal tissues around apex of tooth
30
Functions of apical periodontitis?
Defence - confines bacteria, prevents spread into adjacent bone spaces, bone resorption
31
What are the three different histological presentations of apical periodontitis?
Granuloma, abscess, cyst
32
How to distinguish between a granuloma, abscess and a cyst?
Cannot distinguish clinically or radiographically (only histologically) except if there is a sinus tract then it is an abscess
33
What is the most common histology of apical periodontitis?
Granuloma
34
What is a granuloma?
Inflammatory lesion - lymphocytes, macrophages, plasma, fibroblasts, CT ## Footnote Can be seen on tooth sometimes when extracted
35
What happens histologically during abscess formation?
Change in cellular dynamics - dramatic increase in phagocytic activity and number of PMNs
36
What is a chronic abscess?
Persistent, walled off chronic inflammatory tissue keeps areas of suppuration localised
37
What are cysts?
Epithelium lined cavities that contain fluid or semi-solid material
38
Where do apical cysts originate from?
Epithelial cell rests of Malassez
39
What are the variations in cyst linings?
Continuous, disrupted, missing
40
What is a pocket/bay cyst?
Inflammatory cyst, sac-like, open to and continuous with the root canal space
41
What is a true cyst?
Within the apical granuloma, no connection between cavity and root canal surface
42
Where can cysts of upper teeth originate from?
Maxillary sinus
43
What can we do with Endodontics?
Reduce bacterial levels to negligible, prevent endotoxins from reaching apical tissues, entomb/incarcerate any surviving bacteria, prevent ingress of fluid ## Footnote This leads to the active lesion subsiding and bone regeneration
44
What is the success rate of endodontic treatment in teeth without AP?
83-100%
45
What is the success rate for endodontic treatment in re-treatment cases without AP?
89-100%
46
What is the success rate of teeth with Apical periodontitis?
46-93%
47
What is the success rate for re-treatment cases with AP?
56-84%