EndoBoard Flashcards

1
Q

Q1 : Difference between peritubular dentin and inter-tubular dentin?

A

Peritubular: is highly mineralized 95% with no or little collagen
Inter-tubular: is primarily formed of dense collagen matrix with collagen fibers and it forms the major bulk of the dentin.

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2
Q

Q2 : Why are there differences in the % of reported prevalence of cyst and granulomas?

A

Granulomas and cyst represent different stages of chronic periradicular pathosis. (Liapatas et al, IEJ 2003)
Accurate histopathological diagnosis of radicular cyst can only be achieved through serial sectioning or step-serial sectioning of the lesions removed in toto (Nair et al, OOOE – 1996) and only few studies in which either one of those essential techniques were used (Nair, IEJ 1998, Simon, JOE 1980) while most of the others studies analyzed specimens obtained from wide sources for routine histopathological reports.

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3
Q

Q3 : Does the increase in pulpal pressure due to inflammation result in strangulation of the pulp and pulp necrosis?

A

NO
The strangulation theory has been disproven by van Hassel (OOO – 1971) He showed that the increase in pulpal blood pressure is localized at the area of inflammation and the blood pressure is less 1-2mm away from area of inflammation. This is made possible by 3 main features:
Low compliance environment (pulp is housed by hard dentin) which does not allow further increase in net fluid filtration (tissue pressure) (Heyeraas & Berggreen, Crit Rev Oral Biol Med -1999)
Flow of blood vessel to adjacent tissues: Increase in the pulpal pressure to the critical level (16-20mm/Hg) will open the arterio-venous and venous-venous anastomosis resulting in shunting of the blood.
Lymphatics:
Which collect tissue fluid and tissue protein back to the blood stream.

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4
Q

Q4 : What are the functions of the dental pulp?

A

1) Formation of dentin
2) Repair of dentin (tertiary)
3) Nutrition to avascular dentin
4) Protection (defense)
5) Sensory (pressure & temperature)
6) Hydrates dentin (prevent fracture)

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5
Q

Q5 : Which of the following neuropeptides have the highest concentration in a healthy pulp?
NKA / SP / CGRP / VIP

A

Awawdeh et al (EJ - 2002) investigated the concentration of substance P (SP), neurokinin A (NKA) and calcitonin gene related peptide (CGRP) in painful and healthy human dental pulps. They found that Substance P and CGRP were present in all samples and NKA was detected in 96% of the pulps. They also found that CGRP was present in much higher concentrations than SP and NKA in both painful and non-painful teeth.

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6
Q

Q6 : What is the role of Dendritic cells in the pulp?

A
  • They are Accessory cells of the immune system
  • They are antigen presenting cells (phagocytose antigens, present peptides to the T cells) - They provide necessary signals to activate T-lymphocytes
    (Jontell et al, Crit Rev Oral Biol Med - 1998)
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7
Q

Q7 : Which method can accurately allow proper diagnosis of radicular cysts?

A

Accurate histopathological diagnosis of radicular cysts can only be achieved through serial sectioning or step-serial sectioning of the lesions removed in toto (Nair et al, 000OE – 1996)
Only few studies in which either one of those essential techniques were used (Nair, IEJ - 1998, Simon, JOE - 1980). While most of the others studies analyzed specimens obtained from wide sources for routine histopathological reports.

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8
Q

Q8 : What is the prevalence of periapical cysts compared to granuloma?

A

Lalonde & Luebke (000 - 1968) showed that out of 800 specimens the results showed the following incidence:
Periapical granulomas (45.2%)
Radicular cysts (43.8%)
Such histopathological diagnostic specimens, however, were derived through apical curettage do not represent lesions removed in-toto. Therefore, the diagnosis may not be accurate
Nair et al (OOOE 1996) showed that out of 256 specimens:
- 35% were periapical abscesses
- 50% were periapical granulomas
- 15% were periapical cysts: a) 9% were true cysts b) 6% were pseudocysts

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9
Q

Q9 : Describe the role of neuropeptides in the dental pulp?

A

Neuropeptides are signaling molecules released by stimulated sensory or autonomic (sympathetic or parasympathetic) nerves.
They modulate neural activity as well as vascular and immunological activity within the dental pulp. This all plays a role in the function and repair of the dental pulp. Neuropeptides form the communication between the nerve fibers and the pulpal blood flow. Inflammation will lead to nerve sprouting resulting in increase production of neuropeptide
There are 3 types of neuropeptides:
Sensory derived neuropeptides
1) Substance P (SP)
2) Calcitonin gene related peptide (CGRP)
3) Neurokinine A (NKA) & Neurokinine B (NKB)
They result in vasodilation and increase in capillary permeability and they can also activate inflammatory cell migration.
Sympathetic derived neuropeptides: Neuropeptide Y(NPY)
Which result in vasoconstriction and modulation of the sensory neuropeptides.
Parasympathetic derived neuropeptides: Vasoactive intestinal peptide (VIP)
Result in vasodilatation and can modulate the sympathetic neuropeptides

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10
Q

Q10 : What does the term “proton pump” mean?

A

Proton pump is the pumping of hydrogen ions to make the area more acidic to initiate resorption, this results in dissolution of the hydroxyapatite (inorganic structure). This occurs at the Ruffled border of osteoclasts/dentinoclasts/cementoclasts

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11
Q

Q11 : What are the cells present in the dental pulp?

A

1) Odontoblast (responsible for dentin formation and repair as well as the pro-inflammatory responses)
2) Fibroblast Plays role in the production of the extra-cellular matrix
3) Stem/progenitor cells
4) Defensive cells (macrophages and T cells)
5) Dendritic cells

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12
Q

Q12 : What is the composition of the Dentin organic Matrix?

A

Type I collagen
Type V collagen
Dentin Noncollagenous protein (NCP):
Dentin Sialo Phosphoprotein (DSPP), DSP, and DPP which represent 50% of ECM
NCP with Calcium binding properties (found in dentin and bone)
a) Osteocalcin (OC)
b) Dentin Metalo Protein (DMP1).
c) Bone Sialoprotein (BSP)

NCP synthesized by odontobolast but also present in soft tissue and organs
- Osteonectin
- Osteopontin
NCP not expressed by odontobolast (2HS glycoprotein)
**Growth factors sequestered in the dentin matrix **(BMP, TGFb)

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13
Q

Q13 :What is the intra-pulpal hydrostatics pressure of a healthy pulp?

A

10-28mmHg

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14
Q

Q14 : Explain the difference between primary dentin, secondary dentin and tertiary dentin?

A

Primary dentin: formed by odontoblast previous to tooth eruption
Secondary dentin: formed by odontoblast after tooth eruption (at a slower rate).
Tertiary dentin: formed in response to a localized stimulus of any sort

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15
Q

15 : Describe the hydrodynamic theory and the evidence supporting it?

A

The hydrodynamic theory refers to the rapid outward flow of fluid in the dentinal tubules that is initiated by strong capillary forces resulting in pain stimulation. (Brannstrom, JOE - 1986)

Early work by Brännstrom & Astrom (JDR-1964) hypothesized that fluid movement within the dentinal tubules can be responsible for pain reponses. Later Brannström et al. (Caries Res-1967) showed that heat can cause inward fluid movement. while cold can cause outward fluid movement resulting in distortion of odontoblastic processes and stimulation of nerve responses. Olgart et al. (Acta Odontologica Scandinavica-1974) showed that there is out fluid movment the dentinal tubules. prevent caries from invading the dentinal tubules. Later Narhi et al. (Arch Oral Biol-1982) in a dog model supported the hydrodynamic hypothesis by showing that various stimuli (such as air blast, acid etch and several solutions) would induce fluid flow in dentinal tubules which can result in sensitivity.

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16
Q

Q16 : Which of the following inflammatory cells have the highest representation in a periapical granuloma?

A

Macrophages were the predominant inflammatory cell, followed in descending numerical order by lymphocytes, plasma cells, and neutrophils (Stern et al, JOE-1981)
% of inflammatory cell:
- Macrophages (24%)
- lymphocytes (16%)
- Plasma cells (7%)
- Neutrophils (4%)
Majority of inflammatory cells were macrophages, T and B lymphocytes (Liapatas et al, IEJ-2003)

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17
Q

Q17 : What are the types of terminal nerves present in the pulp-dentin complex?

A

Gunji (Arch Histol Jpn - 1982) classified the terminal nerves in the pulp and dentin into:
1- Marginal pulpal nerve fibers: Runs from the sub-odontoblastic nerve plexus (Plexus of Rashkow) towards the odontoblastic layer but do not reach the predentin (most common fibers).
2- Simple predentin nerve fiber: Reaches or penetrates the predentin border.
3- Complex predentin nerve fiber : Penetrate the predentin border and shows very complicated terminal ramifications.
4- Dentinal nerve fiber: they enter the dentin through dentinal tubules. They can extend up to 200µm (50-100 µm average).

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18
Q

Q18 : What is the compositional differences between a granuloma and a cyst?

A

Granulomas and cysts are structurally very similar. Periapical cyst, however, contain nearly 5 times more epithelial cells than granulomas. In all other cellular parameters, the cysts and granulomas were quantitatively similar (Stern et al, JOE - 1981)

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19
Q

Q19 : Which of the following fibers is the smallest in size?

A

C Fibers size ranges from 0.4-1.2µm in size and their velocity is 0.5-2 m/sec. They are located in the core of the pulp. C fibers have high threshold to stimulus and their response will result in a dull aching pain. Activation of the C fibers indicates a later stage of inflammation (given its location).

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20
Q

Q20 : Describe the role of cytokines in regulating bone resorption?

A

Kawashima & Stashenko (Arch of Oral Bio-1999) evaluate the expression of bone-resorptive and regulatory cytokines in the development of periapical lesions in mice. They showed that:
Th1 cell cytokines (IL-1 α, IL-12, TNF α and INF ϒ) seem to up-regulate inflammatory bone resorption Th2 cells cytokines (IL-4, 6, 10, 13) appears down-regulate bone resorption.

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21
Q

Q21 : Explain how the microvasculature of the pulp help regulating pulpal inflammation?

A

Through the extensive arterio-venous and venous-venous anastomosis which allow regulation of blood flow during inflammation by passing blood from region of inflammation to region of viable cells. This shunting mechanism will regulate the pulp blood flow during injury (Kim, JDR 1985)

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22
Q

Q22 : What is neural sprouting and how does it participate in dental pain?

A

Neural sprouting is an increase in the density of innervation in inflamed tissue that leads to increase in pain sensitivity.
Taylor et al. (Brain research - 1988) showed extensive increases in the number of calcitonin gene-related peptide immunoreactive(CGRP-IR) nerve fibers subjacent to injured root dentin of rat molars suggesting that rapid reversible sprouting of sensory nerve fibers may be an integral part of dentin reaction to injury.

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23
Q

Q23 : How far do the odontoblastic processes extend into the dentinal tubules?

A

The odontoblastic process extend around 1/3 the length of the dentinal tubule. This has been shown by several studies (Holland, J Anat- 1976; Thomas, JDR-1985; Weber & Zaki, JDR-1986). LaFleche et al. (J Biol Buccal - 1985) proposed that dentinal tubules extend only about one-third the distance from the tubule due to a retraction of the process during extraction. The formers, however, believe that LeFleche et al may have been confused by fixation and tissue reparation artefacts.
A more read on this as well as the pulp dentin complex can be viewed in the review by** Pashley (Crit Rev Oral Biol Med - 1996)**

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24
Q

Q24 : Which of the following sensory fibers are not stimulated by EPT?

A

C - Fibers
Narhi et al. (Scand J Dent Res-1979) investigated electrical stimulation of teeth with pulp testers on cats. They found that EPT stimulates only A-beta and A-delta fibers, not C-fibers.

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25
Q

Q25 : What is the difference between A-delta fibers and A-Beta fibers?

A

A fibers are myelinated, fast conduction fibers with low stimulation threshold. They are superficially located in the pulp/dentin junction. They transmit pain directly to the thalamus and generate a sharp and stabbing pain that is easily localized.** (Narhi et al, Proc Finn Dent Soc-1992)**. They are usually the first to react & transmit the pain impulse.
According to Gomes (J Endod Rosario-2011), A-delta fibers represents more than 90% of the A fibers in the pulp. Their diameter range from 2-5 μm and their velocity 12-30 m/sec is activated by hydrodynamic stimuli which lead to rapid fluid movement within the tubules resulting in sharp, piercing pain. The arousal thresholds vary among the A-Delta fiber population.
Low-threshold fibers: cooling & vibration
Higher-threshold fibers: mechanical instrumentation
A-beta fibers is functionally similar to the A-delta fibers but they respond differently to vibration. They are stimulated at a lower electrical threshold and involved in detecting non-noxious stimuli such as vibration and proprioception (pressure and touch); found in the periodontal ligament & oral mucosa. The AB fibers represent 7% of the myelinated fibers entering premolar pulp.
(Figdor, Ann R Australas Coll Dent Surg 1994)

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26
Q

Q26 : Which of the following sensory fibers can maintain their functional integrity in a hypoxic situation?

A

A-Delta Fibers // A-Beta Fibers // B-Fibers // C-Fibers
Oxygen consumption is higher in the thick A fibers than in the thin C fibers, C fibers function for a longer time compared to A fibers in events of injury (Narhi, J Dent Res-1985)

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27
Q

Q27 : What is the difference between reactionary dentine & reparative dentine?

A

Reparative dentin is formed in response to a strong stimulus where the original odontoblasts were destroyed and a newly formed odontoblast-like cells are formed by fibroblasts, that starts forming dentin, which is poorly mineralized and has less tubules. It is also often referred to as “osteo-dentin “due to lack of tubules.

Reactionary dentin is formed in response to decay where the original odontoblast has not been destroyed. Tubules formed are usually not continuous with those of secondary dentin.

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28
Q

Q28 : What is “condensing Osteitis”? and why it develops?

A

It’s a radiopacity at the root apex because of a proliferative bone response to a low-grade chronic irritant.
Green et al (JOE-2013) showed that the histologic changes of condensing osteitis consisted of the replacement of cancellous bone with compact bone. All teeth exhibiting condensing osteitis had an identifiable etiology that likely resulted in degenerative pulp disease.

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29
Q

Q29 : What is the function of the subodontoblastic plexus in the pulp-dentin complex?

A

Exchange of nutrients and waste products between the pulp and the odontoblastic cells

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30
Q

Q30 : Give examples of neuropeptides normally present in the dental pulp?

A

1) Substance P
2) Calcitonin gene-related peptide (CGRP)
3) Neurokinin A
4) Neuropeptide Y
5) Vasoactive intestinal polypeptide (VIP)

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31
Q

Q31 : Describe the basic pulpal protective mechanisms against caries?

A
  • Decrease in dentin permeability: by increasing the deposition of intra-tubular dentine and tubule occlusion by precipitated crystals (Dentin sclerosis) (Pashley, JOPD - 1991)
    Tertiary dentin formation: Acidic by-products of the carious process act indirectly by degrading the dentin matrix and liberating bioactive molecules to stimulate tertiary dentinogenesis. (Smith et al, Adv Dent Res - 2001)
  • Inflammatory and immune reactions. Accumulation of inflammatory cells (accumulation of lymphocytes, leukocytes and exudates) Macrophages are usually the most dominating cells (Brannstrom & Lind, JDR-1965)
32
Q

Q32 : What are the structural compositional differences between plasma and dentinal fluids?

A

Protein concentration is 10% greater in plasma than dentinal fluid
Calcium concentration is 2-3 times higher in dentinal fluids than plasma

33
Q

33 : Which of the following cells represent the highest percentage in a periapical cysts?

A

Vascular elements // Fibroblasts // Inflammatory cells // Epithelial cells
Inflammatory cells comprised slightly more than half the formed elements in periapical cysts or granulomas the others were connective tissue elements. (Stern et al, JOE - 1981)

The % cells is as follows:
a) Inflammatory cells (52 %)
b) Fibroblasts (40%)
c) Vascular elements (6%)
d) Epithelial cells (5%)

34
Q

Q34 : Describe the distribution of the A and C fibers within the dental pulp?

A

A Fibers are located in the pulp-dentin border in the coronal portion of the pulp and concentrated in the pulp horns
C fibers are located in the core of the pulp

35
Q

Q36 : Is there any association between presence of intra-radicular bacterial biofilms & periapical cysts?

A

According to Ricucci & Siqueira (JOE - 2010), intra-radicular biofilms were significantly associated with epithelialized lesions (cysts and epithelialized granulomas or abscesses)

36
Q

37 : Describe the bacterial community in primary endodontic infection and how it is different from secondary infection?

A

According to Siqueira & Rocas (Journal of Oral Microbiology-2009)
Primary infection:
* Mixed bacterial community
* Predominated by anaerobic bacteria
* Diverse number of species in larger numbers are present
* The size of apical periodontitis lesion is proportional to the number of bacteria in the root canal
* Common bacteria in primary infections are Porphyromonas spp, Prevotella spp. Treponema spp. Diolestor spp. T forsythia
Secondary infection:
* Primarily, Gram ve facultative anaerobes
* Less diversity in species and fewer numbers compared to primary endodontic infection
* The number of bacteria in a failed case will vary according to the quality of the treatment (worse treatment more bacteria)
* -E faecalis is predominant in failed cases

37
Q

Q38 : Give examples of methods used to detect microbial species in the root canal system?

A
  • Microscopy
  • Immunological methods
  • Culturing
  • Pyrosequencing analysis.
  • Molecular biology techniques
    a) PCR
    b) RT-PCR (Qualitative)
    c) qPCR (Quantitative)
    d) DGGE
38
Q

Q39 : What are the causes of failure or persistence of an apical infection following endodontic treatment?

A

According to Sundqvist & Figdor (Endo Topics-2003) The contributing factors to persistent infection can be divided in to
1- Intra-radicular infection. Such as missed canal, poor root canal treatment, coronal leakage, isthmus or lateral canals. This is the primary cause of failure in most of the root canal failures. It has been shown by Ricucci & Siqueira (JOE 2010) that intra radicular biofilm is present in 77% of cases with radiographic evidence of apical periodontitis. This percentage further increases in cases with symptoms, sinus tracts, and epithelialized lesions

2- Extra radicular infection. Can be either
a) Extra-radicular biofilm on the external root surface. It has been shown by Ricucci & Siqueira (JOE 2010) that the incidence of extra-radicular biofilm is as low as 6%. This incidence can increase up to 70% in cases with sinus tracts (Ricucci et al 2018)
b) Apical Actinomycosis which can only be successfully treated by apical surgery & curettage of the apical inflammatory lesion (Siqueira, Endo Topics-2003) It has been shown to occur between 2-10% of cases treated through endodontic surgery (Borssén & Sundqvist, Oral Surg- 1981, Hirshberg et al, OOOE 2003,)
3- Cystic lesion. It has been hypothesized by Nair (IEJ-1998) that true cysts may not resolve following endodontic treatment and surgical intervention is required.
4-Foreign body reaction. Presence of entrapped foreign body material from endodontic treatment such as gutta purcha or sealer, or food particles may cause persistent of periapical disease. Clinical studies with long-term follow ups have showed that gutta purcha may retard the healing process but will not cause true failure per say (Molven et al, IEJ-2002, Fristad et al. 2004 Azim et al, IEJ - 2016)
5- Fibrous scar tissue healing. While scare tissue is not a true disease, it can mimic periapical disease radiographically (Nair, IEJ 2006).

39
Q

Q40 : Endotoxins level in primary endodontic infection is higher than that of secondary endodontic infection

A

Endotoxins are released by gram -ve bacteria. Gram -ve obligate anaerobes dominate the root canal space in primary infections (Baumgartner & Falker, JOE-1991) compared to secondary/persistent infections which are dominated by gram +ve bacteria (Chavez de Paz et al. IEJ-2003, Chavez de Paz et al, IEJ - 2004)
Gomes et al (JOE-2012) investigated the level of endotoxins in primary and secondary endodontic infections. They found that teeth with primary endodontic infections had higher levels of endotoxin and a more complex community of gram-negative bacteria than teeth with secondary infections. Endotoxin levels were related to the severity of bone destruction in periapical tissues as well as the development of clinical symptoms in teeth with primary infections.

40
Q

Q41 : What is the prevalence of intra-radicular bacterial biofilms in teeth with apical periodontitis?

A

Intra-radicular biofilms were observed in the apical segment of 77% of the root canals. There is also a higher incidence of biofilms in cases with large periapical lesions. (Ricucci & Siqueira, JOE 2010)

41
Q

Q42 : Which of the following procedures will result in the highest incidence of bacteremia? EXTRACTION

A

All of the above procedures may cause bacteremia. Baumgartner et al. (JOE - 1976) showed that bacteremia is less likely to happen during non-surgical RCT unless teeth were over instrumented.
Debelian et al (Endod Dent Traumatol-1995) even showed that over instrumentation during RCT does not appear to influence the occurrence of bacteremia.
Bacteremia is more likely to occur during surgical endodontic treatment and surgical extraction (Baumgartner et al, JOE - 1977)

42
Q

Q44 : What are the dominating bacterial species in teeth with necrotic pulp/apical periodontitis?

A

Sunqvist (1976) showed that anaerobic bacteria accounted for more than 90% of the isolates bacteria in cases with necrotic pulp.
Fabricus et al. (Scan J Dent Res - 1982) showed that after 7 days of infection: proportion of facultative anaerobic greatly higher than strict anaerobic bacteria. After 90 days of infection, 85% of the bacterial cells from the apical region were anaerobic. After 180 and 1060 days of infection, 95-98% are anaerobic.
Baumgartner & Falkler (JOE-1991) showed that 68% of bacteria isolated from the apical 5mm were strict anaerobes.
Siqueria et al. (JOE-2011) investigated the diversity of the apical endodontic microbiota 187 bactenal species-level with 84 genera, and 10 phyla were identified using pyrosequencing analysis. The most abundant and prevalent phyla were.
Proteobacteria (43%) Firmicutes (25%) Bacteroidetes (9%) Fusobacteria (15%) Actinobacteria (5%)

43
Q

Q45 : Why it is difficult to remove a bacterial biofilm from the root canal space?

A

Explanation:
1) Bacterial biofilms can exhibit metabolic cross feeding (community can exist for longer time)
2) Resistant to intra-canal medication such as Ca(OH)2 (Distel et al, JOE - 2002)
3) Resistance to antibiotics (Stewart & Costerton, Lancet 2001)
4) Can survive deep into the dentinal tubules (Love, JOE=2001)
5) Endodontic instruments are unable to mechanically touch all canal walls, and thus won’t be able to mechanically disrupt biofilms along the entire canal wall (Peters et al, JOE = 2001)

44
Q

Q46 : E fecalis is commonly detected in failed endodontic cases. Describe how E fecalis can resist the various disinfection procedures?

A

a) E. faecalis is able to penetrate dentinal tubules to a deep extent, protects it from the action of instruments and irrigants (Haapasalo & Ørstavik, JDR-1987)
b) Its Proton pump enable E Faecalis to resist High PH (Evans et al, IEJ-2002) as a result it can resist Ca(OH)2 and grow in its presence (Distel et al, JOE-2002)
c) It has the ability to invade tubules and binds with collagen (Love, JOE-2001)
d) Environmental signals can regulate the genetic expression of e faecalis (Jett et al. Clin Microbiol Rev-1994)

45
Q

Q49 : Which species are considered “black pigmented bacteria”?

A

There was a nomenclature change in the 1990’s which affected the taxonomic classification of certain species. Older papers referred to a broader group of ‘Bacteroides’ or ‘black-pigmented’ bacteria. These bacteria are gram negative obligate anaerobes. They were divided into two groups according to their ability to ferment carbohydrates. Prevotella (saccharolytic) and Porphyromonas (asaccharolytic) (Robertson & Smith, JMM - 2009)

46
Q

Q50 : What is the prevalence of Candida species in root canal infections?

A

In a recent systematic review and Meta Analysis of literature by Mergoni et al (JOE - 2018), the cumulative prevalence of Candida spp was 8.2%, which is quite a low value and places some doubt as to the real role of yeasts as pathogens in the majority of endodontic infections. They suggested that Candida may play a role in root canal infections although the body of evidence is not strong.

47
Q

Q51 : What is “Anachoresis”? And can anachoresis cause pulp disease?

A

Anachoresis is the localization of blood-borne bacteria during bacteremia to a site of inflammation. The hpothesis is that bacterial in the blood stream can seed directly into the inflamed pulp via the pulpal blood supply during bacteremia,

Delivanis et al (000-1981) conducted a study on a stagnant fluid in instrumented but not filled root canals of five cats. The fluid was analyzed for possible localization and growth of IV injected bacteria 48 hrs. after injection, all sample obtained from the canals were negative for the tested organism, Delivanis & Fan (JOE-1984) repeated the same study but they also over instrumented the canals to cause bleeding. They found that canals can get infected following over instrumentation, indicating that anacorasis can occur

It was thought that anachoresis can cause pulp disease due to presence of bacteria in the blood stream in the inflamed pulp (Tziatas, JOE-1989) These studies, however, do not prove that the pulp subsequently become necrotic as a direct result of the bacteremia Lin et al (JOE-2006), however, showed that teeth with periapical lesions on one side of the jaw did not serve as toci of infection nor caused infection of teeth with devitalized pulps on the other side of the jaw.
Another argument against anachoresis as a route of pulpal infection comes from the study by Möller et al (Scan Dent Res-1981) were cases of aseptic necrosis remained bacteria-free after 6 to 7 months of observation.
It appears that anachoresis can occur but it does not cause pulp/periapical disease. It can, however, aggravate a periapical condition making it more symptomatic Sabeti et al (JOE-2003) showed that Cytomegalovirus (HCMV), Epstein-Barr Virus (EBV) participates in the pathogenesis of symptomatic periapical lesions which can impairs local defenses, thereby inducing overgrowth of endodontopathic bacteria.

48
Q

Q52 : Does LPS play a role in pulp and periapical disease? Explain

A

YES
Schein & Schilder (JOE-1975) investigated the levels of endotoxin in the fluid aspirated from the root canals of teeth that were opened for RCT. They found that necrotic teeth contained greater conc. of endotoxin than those with vital pulps, symptomatic teeth also contained more endotoxin than asymptomatic teeth. There was also more endotoxins in teeth with PAR compared to teeth without PAR. These results suggested a possible role of endotoxins in pulpal and periapical diseases.
Pitts et al (JOE - 1982), later evaluate the effect of endotoxin on periapical tissue by introducing endotoxin into the root canals of dogs. They found that root exposed to endodontoxins tended to show periapical radiographic changes sooner and to a more severe degree. Histologically, they also showed larger bone defects with more intense degree of inflammation. The results of this study indicate that endotoxins may have a role in periapical inflammation and bone destruction.
Khabbaz et al (OOOE-2001) found that endotoxins were detected in all pulpal tissues of symptomatic & asymptomatic carious teeth. The conc., however, of endotoxins in the pulpal tissue of symptomatic teeth was significantly higher suggesting a possible association of endotoxins levels with severity of pulpal pain.

49
Q

Q53 : Can bacteria survive in the periapical area?

A

Normally bacteria cannot survive planktonically in the apical area. With exception to few species such as actinomcyes (Bystrom et al, Endod Dent Traumatol - 1987)
They can only survive in a biofilm (Plaque) structure on the external root surface (Tronstad et al, Endod Dent Traumatol - 1990). The incidence, however, is very low (4-6%) (Siqueira & Lopez, IEJ-2001), (Ricucci & Siqueira, JOE - 2010)
Several earlier studies have shown the ability of bacteria to survive in the apical area such as Tronstad et al. (Endod Dent Traumatol, 1987), Waymen et al. (JOE-1992) and Iwu et al (000-1990). Since all these were clinical studies, it is possible that these samples were contaminated during sampling despite their careful measurements, since maintaining a surgical sterile environment in the oral cavity is not really possible
Walton & Ardejman (JOE-1994) have shown in a monkey study that when a blocks sections (bone and lesion) were harvested from teeth where apical periodontitis was induced, there were no bacteria found in all samples.

50
Q

Q54 : What are the most commonly detected bacteria in teeth with acute apical abscess?

A

Sakamoto et al. (oral Micro & Immun- 2006) performed a molecular analysis on teeth with asymptomatic apical periodontitis and teeth with acute apical abscess. The species that most commonly isolated in teeth with acute apical abscess were
1-F nucleatum T-RF type II
2-P Intermedia
3- Dialister pneumosintes
Gomes et al (JOE = 2006) showed that Filifactor alocis, Tannerella forsythia, and Treponema denticola were associated with acute apical abscess as well.

51
Q

Q55 : What is a bacterial biofilm?

A

Microorganisms attached to a surface and form 3-dimensional structure held together by extra cellular polymeric substance that can cope with environmental stresses
Holds different types of bacteria
Connected via water channels
Communicate via quorum sensing** (Scoransky & Haffajee, Periodontology 2000-2002)**
Exchange gene coding thereby increasing their microbial resistance.

52
Q

Q56 : Describe the pathogenic role of E. faecalis?

A
  • According to Rocas et al (JOE 2004), E. faecalis possesses certain virulence factors including lytic enzymes, cytolysin, aggregation substance, pheromones, and lipoteichoic acid. It has been shown to adhere to host cells, express proteins that allow it to compete with other bacterial cells, and alter host responses.
  • E. faecalis is able to suppress the action of lymphocytes, potentially contributing to endodontic failure (Lee et al, JOE 2004)
    -E. faecalis is not limited to its possession of various virulence factors. It is also able to share these virulence traits among species, further contributing to its survival and ability to cause disease.
    E. faecalis possesses a proton pump that allows it to adapt to harsh environments (Evans et al., IEJ 2002). This proton pump is theorized to contribute to E. faecalis unique resistance to CaOH2
    Check the review by Stuart et al (JOE-2006) and on Enterococcus faecalis and Its role in root canal treatment failure.
53
Q

Q57 : Describe the differences between endotoxins and Lipoteichoic acid?

A

Endotoxins lipopolysaccharides (LPS) are released by gram-negative bacteria and they are recognized mostly by toll-like receptor 4 (TLR-4) on antigen presenting cells (APC) or macrophage resulting in inflammatory cytokine production and activation of innate immune system.
Lipoteichoic acids (LTAs), on the other hand, are released by gram positive bacteria and they are recognized by TLR 2. They can also induce inflammation but they are not as virulent as LPS.

54
Q

Q58 : How can an extra-radicular biofilm develop?

A

Extra-radicular biofilm can develop either through periodontal infection or endodontic infection spreading through the dentinal tubules and reaching the external root surface.
Recently, Ricucci et al. (JOE-2018) showed that extra-radicular biofilms were more prevalent in cases with chronic apical abscess suggesting that saliva may gain access to the apical root segment through sinus tracts and form bacterial biofilm/calculus on the external root surface.

55
Q

Q59 : Is there any correlation between the bacterial load inside the root canal space and the lesion size?

A

Yes
Ricucci & Siqueira (JOE -2010) showed a higher incidence of bacterial biofilms in cases with large periapical lesions.

56
Q

Q60 : Other than bacteria, what other species can play a role in persistent apical periodontitis?

A

Candida species:
Candida species are normally present in saliva. Baumgartner et al (JOE-2000) evaluated the contents of infected root canals and aspirates of cellulitis/abscesses of endodontic origin. They found that C. albicans may be involved in root canal infections. Siqueira et al. (JOE-2002) showed that C albicans has the ability to colonize dentin while other types of fungal species were unable to, which helped explaining why C. albicans is the fungal species most often found in endodontic infections.
Viruses:
Sabeti et al (Oral Microbiol Immunol-2003) stated that Human Cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) active infections are associated with acute exacerbation of apical periodontitis. They hypothesize that periapical active virus infection can impairs local defenses, thereby inducing overgrowth of endodontopathic bacteria and the clinical flare-up of inflammation.
Later, Slots et al. (IEJ-2004) suggested adding HCMV and probably EBV to the list of putative pathogenic agents in symptomatic periapical disease. More recently, Jakovljevic & Andric (JOE-2014) conducted a systematic review to analyze the evidence indicating that HCMV and EBV can actually contribute to the pathogenesis of periapical lesions. The results of this study failed to establish a statistically significant relationship between HCMV and EBV detection and the clinical features of periapical lesions and the mechanisms of HCMV and EBV reactivation and participation in periapical disease progression remain to be revealed.

57
Q

Q61 : What type of bacteria appears to survive commonly after chemo-mechanical root canal treatment in teeth with apical periodontitis?

A

Chavez de Paz et al (IEJ-2003) showed that the most commonly isolated species chemo-mechanical root canal treatment were:
Gram +Ve (85%)
Lactobacillus spp (22%)
nonmutants streptococci (18%)
Enterococcus spp. (12%)

58
Q

Q187 : What is the success rate of direct pulp capping?

A

Bogen et al (JADA - 2008) showed a 98% success when MTA was used as a direct pulp capping material over a period of 9 years in 53 teeth.
Hilton et al (JDR - 2013) showed a success of 81% with MTA vs 68.5% with Ca(OH)2
Mente et al (JOE-2014) showed as success of 81% with MTA vs 59% with Ca(OH)2

59
Q

Q188 : What are the factors affecting the success rate of direct pulp capping procedure?

A

1.Material: Mente et al (JOE - 2014) found that MTA was superior to Ca(OH)₂ (MTA 80% vs Ca(OH)₂: 60%) as a pulp capping material. Probably that applies to other calcium silicate materials as well. Similar results were showed by Hilton et al (JDR - 2013) and Cho et al (JOE - 2013)
2. Hemorrhage control: Matsuo et al (JOE- 1996) found that ability to control bleeding was a determining factor for the success of direct pulp capping.
3. Exposure site: Cho et al (JOE -2013) found that the exposure site being occlusal exposure site has a better success rate that axial exposure sites. They also showed that pulp capping was more successful in younger patients.
4. Patients’ age: Younger patient has a higher success rate (Cho et al, JOE -2013)
5. Time of placing the final restoration: (<2days) (Hilton et al, JDR - 2013)

60
Q

Q189 : Explain the pulp reaction to Ca(OH)2 or MTA as a direct pulp capping material?

A

Upon contact, Ca(OH)2 or MTA will cause liquefaction necrosis of the superficial layer of the pulp which will be neutralized in deeper layers resulting in coagulative necrosis. This will result in slight irritation of the adjacent pulp tissue and stimulation of vascular and inflammatory cell migration and proliferation (to control and eliminate the irritant). This will lead to migration and proliferation of undifferentiated mesenchymal stem cells to differentiation to odontoblast-like cells causing hard tissue formation** (Schroder, J Dent Res - 1985)**

61
Q

Q190 : Explain why a successful regenerative procedure with initial evidence of root maturation and resolution of periapical pathology may fail on the long run?

A
  1. Reinfection (coronal leakage)
  2. Trauma
  3. Remaining bacteria inside the root canal space.
    Over time, the number of bacteria inside the root canal space may increase resulting in activation of the immune system. This can lead to recruitment of inflammatory meditators and impairment of attachment, proliferation and differentiation of stem cells. This can result no further hard tissue deposition and bone resorption.
    Liu et al (IEJ -2016) has shown that TNF-α and IL-1β can Inhibited mineralization and osteogenic-/ dentinogenic-related gene expression
62
Q

Q191 : What are the current challenges of pulp revitalization/revascularization techniques used today?

A

1- Nb of stem/progenitor cells that we can attract to the root canal space
2- Migration competition between the different types of cells (SCAP, PDLSC, MSC, etc)
3- It’s difficult to clinical identify the presence of viable apical papilla
4- Generated tissues in the canal is not pulp/dentin-like but more bone-like or cementum like
5- Microbial control (achieving a sterile environment) to ensure success and sustainability of the treatment

63
Q

Q192 : What are the current limitations of outcome studies in regenerative endodontics?

A

1- Studies generally have small patient sample size
2- Criteria used to define success are inconsistent.
3- Studies generally have a short follow up time and the sustainability of the outcome may not be guaranteed
4- There is generally a focus on radiographic healing (goal 1) as the primary outcome measure in most of the outcome studies and minimal attention to increase in root thickness/ length (goal 2) and vitality testing (goal 3). Goal 2 and 3 are the main reason why a clinician attempts this procedure in the first place.

64
Q

194 : Describe the structure of the hard tissue barrier formed under direct pulp capping material (MTA or Ca(OH)2)?

A
  • It has tunnel defects (Cox et al, Oper Dent- 1996, Al Hezaimi et al, JOE -2011).
  • It resembles more bone than dentin (Andelin et al, JOE - 2003)
  • Nair et al (IEJ, 2008) showed that the hard tissue barrier formed under MTA is more compact with less pulpal inflammation compared to Ca(OH)2 that had more tunnel defect. Later Al Hezaimi et al (JOE, 2011) showed that there are tunnel defects in the hard tissue barrier in MTA as well, but the defects were more prominent with Ca(OH)2.
65
Q

195 : List the available sources for stem cell sources that can clinically aid in pulp revascularization/ revitalization?

A

Dental pulp stem cells (DPSC) from remaining pulp tissue inside the root canal space
Stem cells of the apical papilla (SCAP) if they are still surviving in the apical tissue
Periodontal stem cells and mesenchymal stem cells (PDLSC, MSC) from the periapical tissue following stimulating apical bleeding
- (MSC) from the blood stream

66
Q

196 : Which of the following treatments have a higher success rate in managing necrotic teeth with open apex: regenerative endodontic procedures or apexification?

A

The existing literature lacks high quality studies with a direct comparison of outcomes of regenerative endodontic treatment and apexification as shown in a recent systematic review by Torabinejad et al (JOE - 2017).
Regen and apexification appear to achieve a comparable outcome in regard to the resolution of symptoms and apical healing (Alobaid et al, JOE 2014; Kahler et al, JOE 2017, Lin et al, JOE 2017). There can have a potential benefit of regenerative endodontic treatment to further increase root length/width (Lin et al, JOE 2017). The procedure, however, has been associated with greater incidence of adverse events (pain, swelling, intervention etc.) was observed in the revascularization procedure (Alobaid et al, JOE 2014)

67
Q

197 : Why is MTA more superior to Ca(OH)2 as a pulp capping material?

A

MTA is non-absorbable and structurally stable compared with Ca(OH)2 products (Al Hezaimi et al, JOE - 2011)
Min et al (JOE - 2008) showed that the hard tissue barrier formed with MTA is thicker and occurred in 100% of the cases compared to Ca(OH)2 (60%). This increase the ability to resist the penetration of microorganism and improves the ability to maintain the integrity of the pulp tissue.
Less inflammation and less tunnel defects in the hard tissue barrier with MTA (Nair et al, IEJ- 2009)
The success rate of MTA was constant over the follow-up period whereas the Ca(OH)2 tended to show failures at 2-3 years (Mente et al, JOE - 2014).

68
Q

198 : What is the difference between “Cell homing” approach and “Cell Based” approach in pulp regeneration?

A

Cell homing: attracting stem cells in the body to the site of interest (root canal space)
Cell based: growing stem cells in-vitro and placing them directly into the root canal space.

69
Q

199 : What is the difference between reparative dentin and reactionary dentin?

A

Reparative dentin: the original odontoblasts are destroyed and newly differentiated odontoblast-like cells are formed by the underlying fibroblasts. The hard tissue formed is generally less tubular or lacks dentinal tubules and more irregular (more bone-like than dentin-like).

Reactionary dentin: is formed by the original odontoblast. Dentin is more regular and tubular than reparative dentine. Tubules are usually are not continuous with those of secondary dentin

70
Q

200 : Explain why the current AAE protocol for pulp regeneration suggests a) Low conc of NaOCI in the first visit (1.5%) b) Ca(OH)2 or Low conc of triple or double antibiotic paste (TAP/DAP) as an intra canal medication c) The use of 17% EDTA as the final irrigation before stimulating bleeding d) The use of CHX is not recommended

A

A. The use of low conc (1.5%) of NaOCI is based on the article of Martin et al (JOE-2014) which showed better survival of the stems cells of the apical papilla (SCAP) and greater dentin sialophosphoprotein (DSPP) expression with 1.5% NaOCI compared to other concentrations.

B. Ca(OH)2 or low conc TAP/DAP as an intra-canal medication
High conc of TAP/DAP has been shown to have a negative effect on the survival of SCAP. Low conc starting 1-6mg/ml has been shown to allow for SCAP survival (Ruparel et al, JOE - 2012). Ca(OH)2 has also been shown by Galler et al (JOE-2015) that it does not interefer with TGF beta release from dentin..

C. The use of 17% EDTA as the final irrigation before stimulating bleeding
EDTA facilitate the release of growth factors from Dentin and allows better survival of stem cells (Galler et al, JOE-2015,Martin et al, JOE-2014)

D. The use of CHX is not recommended
CHX has been shown to have a negative effect on the survival of SCAP (Trevino et al, JOE-2011).

71
Q

What are the “zones of fish”?

A

Zones of Fish were the early attempt to disprove focal infection theory by showing that bone infection can be contained and will not spread to distant organs. (Fish, JADA- 1939)
Zones of fish can be divided into 4 zones:
1) Zone of infection
2) Zone of contamination
3) Zone of irritation
4) Zone of stimulation

72
Q

Q36 : Which of the following sensory fibers are not stimulated by EPT?
A - Delta Fibers / A - Beta Fibers / C - Fibers

A

C Fibers
The unmyelinated C-Fibers of the pulp do not respond during conventional electric pulp testing because they have higher threshold and only intense thermal stimuli that are able to proceed tissue injury can activate them (Trowbridge, JOE 1986).

73
Q

Diagnosis

Q63 : Does orthodontic tooth movement impact the viability of the dental pulp?

A

According to Hamilton & Gutmann (IEJ-1999), orthodontic tooth movement can cause degenerative and/or inflammatory responses in the dental pulp of teeth with completed apical formation. The impact of the tooth movement on the pulp is focused primarily on the neurovascular system, in which the release of neuropeptides can influence both blood flow and cellular metabolism. As a result of that, calcification of the root canal space may occur and pulp testing may be affected
The incidence and severity of these changes may be influenced by previous or ongoing insults to the dental pulp, such as trauma or caries.
In a recent systematic review by Weissheimer et al. (IEJ 2021), they showed that orthodontic movements do not induce loss of pulp vitality. The level of evidence, however, is if low to very low certainty

74
Q

Diagnosis

Q64 : How influential is CBCT imaging in treatment decision-making?

A

CBCT can be very influential in treatment decision-making. It has been consistently showing that it has better capabilities than other imaging modalities in depicting the features of the periapical area (Tsai et al, JOE-2012).
Rodriguez et al. (JOE-2017) investigated the Influence of CBCT in Clinical Decision Making among Specialists. They found that examiners altered their treatment plan after viewing the CBCT scan in 27.3% of the cases. In high difficulty cases, the variation of the treatment plan increases to 52.9%.
In a systematic reveiw by Aminoshariae et al (JOE - 2018), CBCT imaging was reported to have twice the odds of detecting a PAR than traditional PA radiographs in endodontic outcome studies.
Chogle et al. (JOE-2020) showed that CBCT imaging has a significant effect in determining the etiology of endodontic disease (55%) and in recommending treatment (49%)

75
Q

Diagnosis

Q65 : List potential causes of false negative responses to electric pulp testing (EPT)?

A

1- Restorations
2- EPT doesn’t have batteries
3- Trauma (Fulling & Andreasen, Scand J Dent Res - 1976)
4- Open apex (Johnsen et al, JDR - 1985)
5- Calcification of the root canal space (Bender, JOE - 2000)
6- Exposure to head & neck radiation (Garg et al, JOE-2015, Gupta et al, JOE - 2018)
7- Current passing through adjacent tooth (Myers, JOE - 1998)
8- Orthodontic movement (Burnside et al, Angle Orthodontist - 1974)
9- Primary Hyperthyroidism, due to hypercalcemia (Bender, JOE - 2000)

76
Q

Q66 : Please describe the common features of odontogenic dental pain

A
  • Has the hallmark features of inflammatory pain- sharp high intensity and/or dull aching throbbing pain
  • Presence of etiological factors (caries, trauma, restorations).
  • Ability to reproduce chief complaint during examination.
  • Unilateral pain.
  • Sensitivity to percussion, temperature.
  • Pain reduction by local anesthetic administration.