CTB Theme 2 Flashcards

1
Q

what are the 3 phases of tooth development

A

initiation
morphogenesis
histogenesis

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2
Q

what is determined in initiation and how is it characterised

A

the tooth position

appearance of tooth germs

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3
Q

what is determined in morphogenesis and how is it characterised

A

tooth shape

cell proliferation and movement

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4
Q

what is formed in histogenesis and how is it characterised

A

dental tissues

cell differentiation and specialisation (e.g. odontoblasts and ameloblasts)

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5
Q

what occurs firstly in tooth initiation

A

primary epithelial band forms
thickening of oral epithelium
condensation of mesenchymal cells

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6
Q

when is the primary epithelial band formed

A

6 weeks in utero

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7
Q

what causes the thickening of the oral epithelium

A

the cells divide downwards thickening the epithelial band

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8
Q

what are the 2 types of lamina formed in tooth initiation

A

dental and vestibular lamina

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9
Q

in what direction do dental and vestibular lamina form

A

dental - lingually

vestibular- buccally

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10
Q

how is vestibular lamina formed

A

epithelial cells proliferate and the central cells subsequently enlarge and degenerate to produce the sulcus of the vestibule

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11
Q

what occurs in tooth morphogenesis

A

formation of the tooth bud

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12
Q

when is the tooth bud formed

A

8 weeks in utero

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13
Q

what occurs in the bus stage of tooth morphogenesis

A

elongation of dental lamina
formation of localised swellings
condensation of mesenchymal cells surrounding the tooth bud

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14
Q

what occurs in the early cap stage

A

enamel organ develops

cap not completely formed

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15
Q

when does the early cap stage occur

A

11 weeks in utero

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16
Q

when does the late cap stage occur

A

12 weeks in utero

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17
Q

how does the enamel organ form

A

dental epithelium forms a cap shaped structure, the enamel organ

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18
Q

what forms the enamel knot

A

a group of non-dividing epithelial cells

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19
Q

what is the function of the enamel knot

A

a transient molecular signalling centre. can send instructions to surrounding cells to induce changes in shape

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20
Q

what forms the dental papilla

A

condensed mesenchymal cells underlying the enamel organ

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21
Q

what forms dental follicle

A

mesenchymal cells surrounding the enamel organ

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22
Q

what does the dental papilla form

A

pulp

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23
Q

what does the dental follicle form

A

periodontal tissue

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24
Q

when does the early bell stage form

A

14 weeks in utero

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25
Q

what is the enamel organ distinguished by

A

outer enamel epithelium

with cuboidal epithelial cells

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26
Q

what is the stellate reticulum

A

group of star shaped cells in the centre of the enamel organ and synthesise glycosaminoglycans

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27
Q

what are the intracellular spaces filled with when epithelial cells get separated in morphogenesis

A

glycosaminoglycans and collagens I, II, III (ECM)

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28
Q

what are the characteristics of inner enamel epithelium

A

columnar

the epithelial cells differentiate into ameloblasts later

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29
Q

what happens to the mesenchymal cells of the dental papilla and dental follicle in morphogenesis

A

they continue proliferating

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30
Q

what is the stratum intermedium

A

2-3 layers of flat epithelial cells that form between inner enamel epithelium and stellate reticulum

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31
Q

what does the stratum intermedium produce

A

alkaline phosphatase

- mineralisation of enamel matrix

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32
Q

what is the stratum intermedium involved in

A

protein synthesis, transport of substances to and from inner enamel epithelium (epithelium)
-ameloblasts supporting function

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33
Q

what happens to the dental papilla in tooth morphogenesis

A

generates fibroblasts and mesenchymal stem cells of the pulp, and odontoblasts

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34
Q

what happens to the dental follicle in tooth morphogenesis

A

it supports the enamel organ with nutrients and generates tooth supporting tissues

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35
Q

when does the late bell stage occur

A

18 weeks in utero

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36
Q

what happens to the tooth in the late bell stage

A

its acquired its future shape

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37
Q

what happens to the stellate reticulum in the late bell stage

A

it moves downwards which helps protect the cellular area of the developing tooth

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38
Q

what is the cervical loop

A

the growing end of the enamel organ (cell interactions)

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39
Q

where is the cervical loop located

A

where the IEE and OEE meet and is later involved in root formation

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40
Q

what happens when the dental lamina breaks down in the late bell stage

A

enamel organ loses contact with oral epithelium

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41
Q

what are odontoblasts and what do they do

A

they’re dental papilla cells and secrete predentine that mineralises and forms dentine

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42
Q

what are ameloblasts and what do they do

A

they’re inner enamel epithelial cells that secrete preenamel that mineralises and forms enamel

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43
Q

what does the stratum intermedium produce

A

alkaline phosphate and support the enamel

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44
Q

what does the stellate reticulum do

A

protects and maintains tooth shape

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45
Q

what does outer enamel epithelium do

A

maintains tooth shape and exchanges substances with dental follicle

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46
Q

what are the reciprocal tissue interactions in crown formation

A
  • inner enamel epithelium (IEE) separated from dental papilla cells by a cell-free zone
  • IEE cells become elongated and secrete signalling molecules to induce odontoblast differentiation from dental papilla cells.
  • odontoblasts align and produce predentine
  • Signals from odontoblasts (in the predentine) induce differentiation of pre-ameloblasts into ameloblasts that start producing pre-enamel.

Dentine produced first and enamel later due to this interaction

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47
Q

how is the IEE separated from the dental papilla cells

A

by a cell free zone

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48
Q

how is odontoblast differentiation induced from dental papilla cells

A

IEE cells become elongated and secrete signalling molecules to induce odontoblast differentiation from dental papilla cells

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49
Q

how is differentiation of pre-ameloblasts into ameloblasts induced

A

by signals from the odontoblasts in the predentine

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50
Q

what do ameloblasts do

A

produce pre-enamel

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51
Q

is dentine or enamel produced first? why?

A

dentine, as signals from odontoblasts are what cause ameloblast formation

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52
Q

how is the crown protected after completion

A

root formation begins

reduced enamel epithelium(REE)

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53
Q

how is REE formed

A

from flattened ameloblasts and remnants of the enamel organ

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54
Q

how does REE protect the tooth crown after completion

A

protects enamel of erupting tooth from being attacked by osteoclasts which remodel the jaw bone once the tooth erupts

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55
Q

how is enamel space caused

A

by demineralisation of enamel during tissue processing

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56
Q

pre-enamel is only partially mineralised, what does this mean for the enamel proteins after demineralisation

A

they remain afterwards

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57
Q

in which direction do successional tooth germs of the permanent teeth bud off from the dental lamina, and what happens to them

A

lingually (not molars)

they stay dormant until further tooth development is initiated

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58
Q

how are permanent molars formed since they have no primary predecessors

A

they are formed by posterior growth of the dental lamina

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59
Q

what does the backward extension of dental lamina give off in the formation of permanent molars

A

gives off epithelial buds which form the molars

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60
Q

when are the first molars formed

A

4 months in utero

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61
Q

when are the second molars formed

A

6 months in utero

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62
Q

when are the third molars formed

A

4-5 years after birth

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63
Q

what are the components of the tooth germ

A

enamel organ
dental papilla
dental follicle

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64
Q

what are the cells of the enamel organ

A
cervical loop
outer enamel epithelium 
stellate reticulum 
stratum intermedium
inner enamel epithelium
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65
Q

what are the cells of the dental papilla

A

odontoblasts
undiff. mesenchymal cells
fibroblasts

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66
Q

what are the cells of the dental follicle

A

cementoblasts
fibroblasts
osteoblasts

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67
Q

what are ex of ectodermal appendages

A
mammary glands 
salivary glands 
teeth 
hair 
tongue papillae
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68
Q

what is the function of the enamel knot

A

signalling centre determining the shape of the tooth

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69
Q

what does the number of enamel knots correspond to

A

the number of cusps

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70
Q

how can an experiment be carried out to determine the odontogenic potential

A
  • dissection of mandibular arch
  • enzymatic digestion to isolate epithelial and mesenchyme
  • recombination of epithelium and mesenchyme followed by in vitro culture
  • transplantation of tooth germ into kidney capsule and in vivo culture for 2-3 weeks
  • tissue analysis
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71
Q

what is meant by the odontogenic potential

A

capability of a tissue to induce gene expression in an adjacent tissue and to initiate tooth development

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72
Q

where is the odontogenic potential at the initiation stage

A

its on the epithelium (epithelial signalling)

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73
Q

where is the odontogenic potential at the bud stage

A

is on the mesenchyme

mesenchymal signalling

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74
Q

how do we know that the odontogenic potential for the initiation stage is on the epithelium

A

because after 11 days there is no tooth formation when dental mesenchyme instructs non-dental epithelium, however there is tooth formation when the dental epithelium instructs the non-dental mesenchyme

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75
Q

how do we know that the odontogenic potential for the bud stage is on the mesenchyme

A

because after the 13 days, when the bud has formed, the dental epithelium cannot instruct the non-dental mesenchyme to form a tooth, however after 13 days the dental mesenchyme can instruct the non-dental epithelium

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76
Q

how is a transcriptional response induced in the dental mesenchyme

A

by overlapping gradients of the morphogens: FGF, BMP in the dental epithelium

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77
Q

what does the initiation stage signalling determine

A

tooth position

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78
Q

which cells will form a tooth

A

only those that express PAX 9

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79
Q

what does mesenchymal signalling by the dental mesenchyme in the bud stage secrete and induce

A

secretes signalling molecules (FGF, BMP) and induces the formation of the enamel knot in the dental epithelium

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80
Q

what signalling occurs in the cap stage

A

enamel-knot signalling

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81
Q

what does enamel knot signalling induce

A

cell cycle arrest within the enamel knot but induces cell proliferation in surrounding cells

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82
Q

which signalling molecules induce cell cycle arrest & proliferation (2 separate molecules)

A

BMP- cell cycle arrest

FGF- cell proliferation in surrounding cells

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83
Q

where does FGF bind in the cap stage

A

to epithelial cells bordering the enamel inducing cell proliferation directed downwards

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84
Q

in which key genetic regulator would tooth development be arrested at an early stage to give rise to Ectodermal dysplasia

A

EDA1/EDAR

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85
Q

in which key genetic regulator would tooth development be arrested at an early stage to give rise to hypodontia

A

PAX9 and MSX1

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86
Q

what is the odontogenic homeobox code tell

A

a hypothesis for specification of tooth identity

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87
Q

what is the evidence for an odontogenic homeobox code

A

mandibular molars will still form if you remove the DLX gene for maxillary molars as they have different genes which can compensate for the loss of DLX 1 and 2
Also an expressed molar gene Barx 1 in the incisor region will transform the incisor into a molar as it overrides the Msx1 incisor gene

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88
Q

what do defects during initiation affect

A

tooth number and identity

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89
Q

what are examples of defects that have occurred during initiation

A

ectodermal dysplasia, hyperdontia

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90
Q

what do defects during morphogenesis affect

A

tooth number, shape and size

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91
Q

what are examples of defects that have occurred during morphogenesis

A

hypodontia, hyperdontia

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92
Q

what do defects during cell differentiation and histogenesis affect

A

hard tissue formation

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93
Q

what are examples of defects that have occurred during cell differentiation and histogenesis

A

amelogenesis imperfecta, dentinogenesis imperfecta

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94
Q

what other dental anomalies can various cellular defects cause

A

eruption
replacement
tumours

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95
Q

what are examples of defects that have occurred as a result of various cellular defects

A

osteopetrosis
eruption cysts
odontomes

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96
Q

what are characteristics of early defects (development)

A

missing teeth
supernumerary teeth
abnormalities of tooth shape and size

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97
Q

what are examples of late defects (cell differentiation)

A

anomalies in structure of teeth-dentine
anomalies in structure of teeth- enamel
anomalies of teeth eruption and/or resorption

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98
Q

what are syndromic defects

A

dental defects seen in combination with other anomalies

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99
Q

what are non-syndromic defects

A

dental defects are not associated with other anomalies (only the dental tissue is affected

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100
Q

what is associated with non-syndromic hypodontia and oligodontia

A

missing teeth e.g.

premolars, lateral incisors, peg shaped tooth

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101
Q

what is associated with syndromic oligodontia

A
Hypohidrotic ectodermal dysplasia (→ Eda1)
Rieger syndrome(→ Pitx2)
Oligodontia-colorectal cancer syndrome (→ Axin2)
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102
Q

which teeth are most likely to be missing caused by MSX1 mutation

A

5s and 8s

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103
Q

which teeth are most likely to be missing caused by PAX9 mutation

A

7s and 8s

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104
Q

what is the multidisciplinary team approach to manage hypodontia

A
Orthodontist 
Child Dental Health dentist 
Restorative dentist
Maxillofacial Surgeon Psychologist
Geneticist
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105
Q

what are treatment options for hypodontia

A

open spaces for bridges or implants

close spaces using orthodontic devices

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106
Q

what gene mutation causes hyperdontia (supernumerary teeth)

A

RUNX2

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107
Q

what occurs in hyperdontia

A

bone defects and craniofacial malformations
enamel hypoplasia, delayed eruption, malocclusion
Dentigerous cysts

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108
Q

normally, what happens to the dental lamina at the bell stage

A

it breaks down

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109
Q

what happens if there is incomplete removal of epithelial remnants

A

supernumerary teeth
eruptions cysts
odontomes (bening tumours)

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110
Q

what do eruption cysts do

A

they block the eruption pathway

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111
Q

what happens if remnants of dental lamina are not removed

A

they can receive signals from the dental follicle and abnormal cysts can form

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112
Q

what is an odontome composed of

A

bone, dentine, soft tissue

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113
Q

what is hypoplasia

A

affects enamel matrix formation- reduced enamel thickness

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114
Q

what is hypomineralisation

A

normal enamel thickness but decreased enamel thickness

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115
Q

what is hypomaturation

A

normal enamel thickness but mottled and softer

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116
Q

what are the inheritance patterns for amelogenesis imperfecta

A

autosomal dominant
autosomal recessive
x-linked forms

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117
Q

what are the gene mutations in amelogenesis imperfecta

A

AMELX, ENAM, MMP20, KLK4, DLX3, FAM83H, WDR72

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118
Q

what is dentinogenesis imperfecta

A

defects in dentine formation (odontoblasts)

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119
Q

what do teeth look like in dentinogenesis imperfecta

A

Blue-gray or amber brown, opalescent teeth

Bulbous crowns and short narrow roots; obliterated pulp chambers

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120
Q

what is the dentine like in dentinogenesis imperfecta

A

Soft dentine => Enamel chipping => Teeth wear down rapidly

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121
Q

what are the inheritance patterns for dentinogenesis imperfecta

A

autosomal dominant

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122
Q

what are the gene mutations in dentinogenesis imperfecta

A

DSPP (DSP, DGP, DPP)

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123
Q

how can dentine be classified

A

by time of development or by anatomical location/histology

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124
Q

what are the types of dentine that develop over time

A

pre-dentine
primary dentine
secondary dentine
tertiary dentine

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125
Q

what is pre-dentine

A

an unmineralised dentine matrix secreted by odontoblasts

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126
Q

what is primary dentine

A

all dentine until the completion of root formation

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127
Q

when does secondary dentine form and what is it associated with

A

after root completion/eruption

ageing- in time it will reduce the pulp chamber and root canal size

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128
Q

when is tertiary dentine produced

A

in response to an external stimuli (attrition, caries, cavity preparation etc).

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129
Q

what is tertiary reactionary dentine

A

when original odontoblasts function in dentine deposition , produce few tubules (slow response=weak stimuli/injury)

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130
Q

what is tertiary reparative dentine

A

when odontoblasts die and are replaced by newly recruited odontoblast-like cells induced from pulp stem cells. deposit dentine with very little structure (rapid response=severe injury)

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131
Q

what are the types of dentine that can be classified by anatomical location/histology

A

coronal dentine

root dentine

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132
Q

what are the types of dentine classified by anatomical location

A
coronal dentine (in crown) 
root dentine
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133
Q

what are the types of coronal dentine

A

mantle dentine

circumpulpal dentine

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134
Q

what is mantle dentine

A

outermost layer of crown dentine, forms first

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135
Q

what is circumpulpal dentine and what are its 4 types

A

forms the bulk of the crown

  • interglobular dentine
  • intertubular dentine
  • intratubular/peritubular dentine
  • sclerotic dentine
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136
Q

what is interglobular dentine

A

a type of circumpulpal dentine- it forms when dentine is mineralised rapidly

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137
Q

what is intertubular dentine

A

a type of circumpulpal OR root dentine - it forms between dentinal tubules

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138
Q

what is intratubular/peritubular dentine

A

a type of circumpulpal OR root dentine- forms inside dentinal tubules

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139
Q

what is sclerotic dentine

A

a type of circumpulpal OR root dentine - caused by complete obliteration of dentinal tubules

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140
Q

what are the layers of root dentine

A

Hyaline layer

Granular layer of Tomes

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141
Q

what is the Hyaline layer

A

the outermost layer of root dentine

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142
Q

what are the chemical properties of dentine (by weight)

A

70% inorganic: calcium hydroxyapatite crystals
20% organic: mainly collagen fibrils
10% water

its less mineralised than enamel

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143
Q

where do hydroxyapatite crystals form and how do they appear (inorganic matter)

A

form between type 1 collagen fibrils

appear as uniform small plates (smaller than those in enamel)

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144
Q

what type of collagen forms in the organic matrix

A

mainly type 1 collagen (90%) and some type III- rest are traces of type V and VI

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145
Q

how do type I and type III collagen form a network

A

type I are linear and type III are reticular which link them together

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146
Q

what makes up the organic matrix

A
collagen fibrils 
proteoglycans 
glycoproteins 
phosphoproteins 
growth factors
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147
Q

what are the glycoproteins involved in the mineralisation process of dentine

A

osteonectin, osteopontin and dentine sialoprotein (DSP)

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148
Q

what are the phosphoproteins in the organic matrix of dentine

A

dentsialoprotein
dentoglyco protein
dentphospho protein

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149
Q

what gene makes the 3 phosphoproteins in the dentine organic matrix and how

A

dentine phosphoprotein gene (DPP) via proteolytic cleavage

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150
Q

what are the growth factors in the dentine organic matrix and what is their function

A

transforming growth factors (TGF)
bone morphogenic proteins (BMP)
released and travel down tubules and stimulate repair in caries

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151
Q

what are the properties of dentine

A
softer than enamel 
higher tensile strength than enamel 
more resilient (elastic) than enamel (supports brittle enamel) 
porous (dentinal tubules) 
sensitive (pulp innervation) 
reactive to damage (tertiary dentine)
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152
Q

how can pulp dentine respond to structure and physical properties especially changes with age

A

its a living organ

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153
Q

how does dentine appear on a radiograph compared to enamel

A

its less radiopaque

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154
Q

how does the dental pulp appear on a radiograph

A

radiolucent

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155
Q

when does dentine formation begin

A

at the late bell stage at the cusp tip

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156
Q

what are odontoblasts

A

mesenchymal cells derived from dental papilla (form dental pulp), they differentiate when receiving molecular signals from pre-ameloblasts

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157
Q

what is a sub odontoblast cell

A

a daughter cell from the division of ectomesenchymal which HAS NOT been exposed to epithelial influence to differentiate into an odontoblast

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158
Q

what is the first step in the formation of pre-dentine

A

formation of large von Koff’s fibres (type III collagen) at 90 degrees angle to the EDJ

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159
Q

what occurs after the formation of von Koff’s fibres in dentinogenesis

A

odontoblasts odontoblast secrete smaller type 1 collagen fibres parallel to the EDJ

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160
Q

what occurs after smaller type 1 collagen fibres are secreted in dentinogenesis

A

the odontoblasts secrete matrix vesicles (mv) than contain highly concentrated calcium phosphate ions (mineralisation)

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161
Q

what is the unmineralised area between the odontoblast layer and mineralising front termed

A

pre-dentine

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162
Q

what do odontoblasts develop in dentinogenesis

A

cell processes

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163
Q

where does initiation of mineralisation in dentinogenesis occur

A

within the matrix vesicle

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164
Q

how is the mineralising front formed in dentinogenesis

A

mineralisation occurs within the matrix vesicle secreted by odontoblasts, causing crystallites to burst out and form the mineralising front

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165
Q

what are matrix vesicles and where are they secreted

A

small (25-250nm) membrane bound vesicles produced by odontoblasts, its secreted into the dentine matrix surrounding odontoblasts

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166
Q

what do matrix vesicles contain

A

phospholipids that bind to calcium

alkaline phosphates

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167
Q

what do the alkaline phosphates from matrix vesicles do

A

increase phosphate concentration and destroys the inhibitor of mineralisation (pyrophosphate)

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168
Q

are matrix vesicles involved in the mineralisation of circumpulpal dentine

A

they have only been observed during mineralisation of mantle dentine. Therefore, they may or may not be involved with mineralisation of circumpulpal dentine

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169
Q

what suggests that collagen is not responsible for initiating mineralisation

A

there is no mineralisation in or near the collagen fibres

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170
Q

why does the thickness of predentine remain constant

A

because the amount that calcifies is balanced by the addition of new unmineralised matrix

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171
Q

what are the 2 patterns of dentine mineralisation

A

linear or globular depending on the speed of dentine formation

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172
Q

where is globular calcification found

A

in the mantle dentine, where the mineralisation occurs by the matrix vesicles

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173
Q

what type of calcification is found in the circumpulpal dentine

A

linear and globular calcification both occur depending on the rate of dentine deposition

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174
Q

when dentine deposition is fast, what mineralisation occurs in circumpulpal dentine

A

globular

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175
Q

when dentine deposition is slow, what mineralisation occurs in circumpulpal dentine

A

linear

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176
Q

what forms within the collagen matrix in globular calcification

A

calcospherites (globular masses of mineralised dentine)

they form within collagen matrix and increase in size until they fuse to form a single calcified mass

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177
Q

what happens if globular calcification proceeds fast

A

incomplete fusion of calcospherites results in formation (of the hypomineralised) interglobular dentine

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178
Q

where can interglobular dentine be found

A

in the upper third of circumpulpal dentine

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179
Q

what are enamel spindles

A

formed from an odontoblast process that has intercalated between two ameloblasts and extends into the enamel (it doesnt follow the path of enamel prisms)

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180
Q

what is enamel tuft

A

hypomineralised region in the enamel which follwos he

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181
Q

what does the scalloping of dentine allow for

A

increased surface area of the EDJ which enables a tighter interlocking between enamel and dentine

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182
Q

what does the excessive branching of dentinal tubules at the EDJ allow for

A

increased sensitivity as the odontoblast processes are involved in sensation of whats going on outside of the tooth

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183
Q

what are the types primary curvature of dentinal tubules

A

s-shaped

linear

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184
Q

where do s-shaped dentinal tubules occur and why

A

in coronal dentine due to the crowding of the odontoblasts because they are pushed apically as dentine grows inwards towards the pulp

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185
Q

where do linear dentinal tubules occur and why

A

in the cervical dentine of the crown and in root dentine because little or no crowded results from decrease the surface areas, and tubules run in a straight course

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186
Q

what is the secondary curvature of dentinal tubules

A

slight changes in tubule direction during dentine deposition creating wavy tubules

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187
Q

what are the 2 types of dentine incremental growth lines

A

von Ebner lines -short period/daily

Adresen lines - long period

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188
Q

what are the characteristics of von Ebner lines

A
daily 
equivalent to cross striations in enamel 
weakiler defines with a closer spacing 
dentine deposited daily 
each line is 3-4 microm
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189
Q

what are the characteristics of Andresen lines

A
long period
equivalent to striae of Retzius in enamel
more sharply defined with wider spacing 
each line 20 micrometers 
6-10 short period lines
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190
Q

when does a contour line of Owen form in dentinal tubules

A

when secondary curvature is pronounced and coincides in adjacent tubules

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191
Q

what causes a contour line of Owen form

A

metabolic stress during dentine formation

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192
Q

what are owen lines

A

accentuated incremental growth lines (von Ebner lines) and are hypomineralised

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193
Q

what is the most prominent incremental growth line

A

the neonatal line due to the disturbances of dentine formation by the birth process

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194
Q

what do the accentuated owen lines correspond to

A

accentuated lines in enamel

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195
Q

where is secondary dentine found

A

mostly on roof and floor of pulp chamber

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196
Q

what is intratubular dentine (peritubular)

A

forms within the dentinal tubule and lines the inner surface as a hyper mineralised layer of dentine (40% more mineralised than the surrounding dentine)

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197
Q

what is intertubular dentine

A

can be any primary or secondary dentine
dentine between the dental tubules
contains a dense network of type I collagen fibrils in which HA are deposited
less mineral than intratubular dentine

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198
Q

what is sclerotic dentine

A

continued formation of intratubular dentine leads to obliteration of the dentinal tubules. if complete the dentine is termed sclerotic dentine

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199
Q

why does sclerotic dentine appear transparent in ground sections

A

due to increased mineralisation

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200
Q

what are dead tracts

A

when dentinal tubules have lost their odontoblast processes following death of odontoblasts or retraction of processes, the tubules become empty and air-filled, and appear as a dark lines in ground sections

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201
Q

why does sclerotic dentine increase with age

A

in areas of attrition & caries of the enamel => Protection of the pulp against invading microorganisms.

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202
Q

what are the two explanations for Tomes’ granular layer

A
  1. extensive branching and backward looping of odontoblast processes
  2. incomplete fusion of calcospherites
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203
Q

when does amelogenesis occur

A

at the late bell stage, morphological changes occur in the enamel organ

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204
Q

how do Inner enamel epithelium cells differentiate into ameloblasts

A

receive signals from odontoblasts (in the predentine)

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205
Q

once ameloblasts are formed what do thy do

A

secrete enamel matrix which forms the aprismatic initial enamel layer

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206
Q

what 2 events can amelogenesis be characterised by

A

enamel secretion

enamel maturation

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207
Q

what occurs in enamel secretion in ameolgenesis

A

enamel matrix secreted by ameloblasts is partially mineralised (30%)

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208
Q

what occurs in enamel maturation in amelogenesis

A

When enamel is fully formed, the mineral content increases to about 96%. Enamel crystals grow wider & thicker at the expense of the organic content and water which is gradually removed

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209
Q

wha are the 3 stages for the life cycle of ameloblasts

A

presecretory
secretory
maturation

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210
Q

what can the presecretory stage be divided into in amelogenesis

A

morphogenetic stage

histodifferentiation stage

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211
Q

what can the secretory stage be divided into in amelogenesis

A

Initial secretory stage without Tomes’ process

Secretory stage with Tomes’ process

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212
Q

what can the maturation stage be divided into in amelogenesis

A

Ruffle-ended ameloblasts
Smooth ended ameloblast
Protective stage

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213
Q

what occurs in the morphogenetic phase in amelogenesis

A

IEE cells have a cuboidal shape
basal lamina produced by IEE separates IEE from the dental papilla
late bell stage: predentine produced by odontoblasts, ameloblast differentiation

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214
Q

what occurs in the differentiation phase

in amelogenesis

A

IEE cells differentiate into ameloblasts

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215
Q

what happens to the pre-ameloblasts in the differentiation phase of amelogenesis

A

Preameloblasts elongate and become columnar; cell nuclei are located proximally towards the stratum intermedium (→ establishment of polarity)

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216
Q

when ameloblasts are fully differentiated what do they do

A

synthesise enamel proteins

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217
Q

what happens to the basal lamina in the differentiation phase of amelogenesis

A

Basal lamina between ameloblasts and odontoblasts is removed as its where dentine and enamel have formed

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218
Q

what occurs in the initial secretory stage of amelogenesis

A

Ameloblasts elongate and secrete enamel matrix, form an (aprismatic) initial layer of enamel
Enamel has lines, not enamel prisms (as its produced by ameloblasts without tomes process)

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219
Q

what occurs in the secretory stage of amelogenesis

A

the ameloblasts form tomes’ process (proximal and distal portion)

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220
Q

what does the proximal portion produce in the secretory stage of amelogenesis

A

interprismatic enamel (‘interrod’ enamel)

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221
Q

what does the distal portion produce in the secretory stage of amelogenesis

A

produces prismatic enamel (‘rod’ enamel)

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222
Q

what happens when the outermost layer of enamel is formed in the secretory stage of amelogenesis

A

Ameloblasts become shorter, lose the distal portion of Tomes’ process → form a thin aprismatic enamel layer (similar to the initial enamel layer)

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223
Q

what happens as the enamel thickness increases in the secretory stage of amelogenesis

A

Distal portion of Tomes’ process develops from proximal portion. It elongates, becomes thinner and is located between prismatic & interprismatic enamel

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224
Q

what are the enamel matrix components

A

amelogenins

non-amelogenin proteins

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225
Q

what are the characteristics of amelogenins

A

90% matrix component
Low molecular weight
roles in regulating growth and thickness of enamel crystals
Form nanospheres
Selectively removed by proteolytic enzymes
provides scaffolding allowing controlled mineralisation of enamel

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226
Q

what proteolytic enzymes are amelogenins removed by

A

enamelysin (MMP20) and kallikrein 4

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227
Q

what are the characteristics of non-amelogenin proteins

A

secreted first but rapidly processed by proteolytic enzymes
10% of matrix content
Form the enamel sheath
Larger proteins: Ameloblastin (70 kDa), Enamelin
amelotin

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228
Q

what is the function of ameloblastin

A

facilitates adhesion of ameloblasts to enamel matrix

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229
Q

what is the function of enamelin

A

promotes and guides formation of enamel crystals; least abundant protein

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230
Q

what is amelotin

A

basal lamina protein; involved in adhesion of junctional epithelium to enamel

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231
Q

how is the maturation stage of ameolgenesis characterised

A

by growth in width and thickness of pre-existing crystals (hardening of enamel)

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232
Q

what are the phases of the maturation phase in amelogenesis

A

transitional phase
maturation proper (phase)
cyclic modulation of ameloblasts

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233
Q

what occurs in the transitional phase of maturation

A

After the enamel layer has been fully formed:

  • Decrease in height & volume of ameloblasts
  • 50% ameloblasts die by apoptosis
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234
Q

what occurs in the maturation proper phase of maturation

A

Removal of water and proteins from the enamel matrix

Transport of ions is required for the increase in mineral content

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235
Q

what occurs in the cyclic modulation of ameloblasts in maturation

A

ruffle-end and smooth-ends alternate

this increases mineral content (ruffle ended) and removal of organic matrix (smooth-ended)

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236
Q

how do ruffle ended (80%) ameloblasts allow selective transfer of calcium ions into the enamel and prevent material in interstitial space

A

there leaky junctions between ameloblasts at proximal (basal) end; tight junctions at distal (enamel) end;

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237
Q

what are the characteristics of smooth ended ameloblasts

A

20%
leaky junctions at distal end
enamel protein fragments and water leave the maturing enamel
trace elements

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238
Q

where does the ISF travel in smooth ended ameloblasts

A

leaks into enamel layer – when cells pump positive ions into a place this is accompanied by H+ which decrease the pH

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239
Q

what do the trace elements in the ISF do (smooth ended ameloblasts)

A

e.g. strontium and fluoride enter the enamel layer and increase hardness

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240
Q

where is the enamel layer most mineralised

A

at the occlusal surface

mineralisation decreases towards the EDJ

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241
Q

why are primary teeth less mineralised than permanent

A

because the maturation phase is shorter

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242
Q

what contributes to the dynamic cycle of enamel demineralisation and remineralisation

A

acid (from food, stomach or of bacterial origin) causes mineral loss

bicarbonate ions from saliva cause remineralisation (pH buffering), allows other ions like fluoride to incorporate into the tissue

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243
Q

what occurs in the protective stage of amelogenesis

A

reduced enamel epithelium(REE) forms inactive (cuboidal) ameloblasts and remnants of the enamel organ (‘papillary layer’)

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244
Q

what does the REE do

A

it covers the tooth crown and protects the enamel from being resorbed by osteoclasts that resorb bone as part of the eruption process or from abnormal cementum deposition

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245
Q

what is the additional function REE has in tooth eruption

A

forms the junctional epithelium

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246
Q

what are the clinical issues of fluoridation? how is this seen histologically

A

excessive consumption- “fluorosis”

  • faint white opacities/severe pitting and discolouration
  • histologically, high porosity in the outer third of the enamel
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247
Q

what are the benefits of water fluoridation

A

incorporation of fluoride ions into enamel crystals

enamel becomes more resistant to acid so reduction of dental caries

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248
Q

what is etching the enamel surface with acid beneficial for

A

adhesive dental restorative materials when removing plaque or a thin layer of enamel which would increase the surface area and create a better bonding surface for adhesive materials

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249
Q

what are white spot lesions due to

A

localised demineralisation of the enamel surface near the gingival margin or fissures
(can be arrested or progress to cavity formation)

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250
Q

when would abnormal enamel formation affect all teeth

A

ameogenesis imperfect, fluorosis

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251
Q

when would abnormal enamel formation affect individual teeth

A
  • local (non-systemic) causes e.g. trauma or unknown aetiology.
  • systemic causes affecting the teeth developing at time of this disturbance e.g. chronological /linear enamel hypoplasia, molar-incisor hypoplasia
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252
Q

how does enamel hypoplasia appear

A

as a groove or pit on the enamel surface

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253
Q

what does enamel hypomineralisation appear as

A

smooth surface but abnormal colour (less mineral; abnormal maturation)

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254
Q

what enamel defects affect all teeth caused by enviro/systemic factors

A

febrile disease
treatments with tetracycline
a chronic ingestion of fluoride ions

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255
Q

how does treatment with tetracycline cause enamel defects

A

it can be incorporated into mineralising tissues resulting in band or total brown pigmentation

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256
Q

what are enamel defects that affect all teeth caused by genetic factors

A

syndromic vs non-syndromic

pattern of inheritance: autosomal or x-liked, dominant or recessive

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257
Q

what is molar hypomineralisation (MIH)

A

associated with opacities and loss of enamel affecting teeth in the first year of life, the molars are fragile and can develop caries easily

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258
Q

when MIH more common

A

in children who have taken amoxicillin in the first year of life , usually for otis media

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259
Q

how does amoxicillin interfere with enamel

A

amoxicillin interferes with ameloblast function at the secretory stage and the temporal sequence of amelogenesis events.

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260
Q

what is linear enamel hypoplasia

A

It is a disruption to enamel formation that causes deep grooves forming on the surface of the tooth. Generally caused by poor nutrition during tooth development

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261
Q

what is the general structure of enamel

A

highly mineralised
96% inorganic contain
4% organic content and water

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262
Q

what origin is enamel

A

epithelial

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263
Q

what are the 2 steps in amelogenesis

A

1st formed enamel is only partially mineralised (30%)

the crystals grow whilst the organic matrix and water are lost

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264
Q

how does the thickness of enamel vary

A

it varies in thickness over different locations (thickest in . cusps, thinnest over cervical margin)
it varies in thickness between different teeth (increase from 1st to 3rd)
enamel is thicker in primary vs permanent

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265
Q

what are the properties of enamel

A
translucent 
extremely hard 
lacks resilience
brittle 
resistant to abrasion 
resistant to sharing and impact forces 
low tensile strength
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266
Q

what are the components of enamel

A

96% mineral- calcium hydroxyapatite (HA)
3% organic - proteins
1% water

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267
Q

what do the HA crystallites combine to form

A

prisms separated by the inter-prismatic region

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268
Q

why is it clinically important to be aware that enamel is brittle and it is supported by the underlying dentine

A

when considering caries and cavity preparation

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269
Q

what is the orientation of the crystals in enamel like

A

not entirely uniform and differ for the prism and interprismatic region

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270
Q

wha are enamel prisms

A

the structural unit of enamel, millions in enamel (each prism=1 ameloblast)

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271
Q

where do enamel prisms grow from

A

the EDJ to the crown surface in layers

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272
Q

what are the three enamel prism patterns in cross section

A
  1. prisms circular
  2. prisms stacked
  3. keyhole pattern
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273
Q

which enamel prism pattern predominates in humans

A

3- keyhole

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274
Q

what is pattern 1 of enamel prisms

A

form with discrete rods surrounded by interprismatic enamel

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275
Q

what is pattern 2 of enamel prisms

A

discontinuities- rods in vertical rows with interrow sheets of interprismatic enamel

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276
Q

what is pattern 3 of enamel prisms

A

horseshoe shaped (keyhole); interprismatic attached to the tail below the head of the prism when seen in cross section

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277
Q

what does the keyhole pattern look like in cross section

A

a wide head towards coronal/occlusal surface

a narrow tail towards cervical

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278
Q

how many ameloblasts is each keyhole rod formed by

A

4
1- head
3- tail

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279
Q

what is the orientation of the crystals within the prism

A

parallel to the long axis of prism in head

oblique to the long axis of prism in tail (angled)

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280
Q

what does the prism sheath form

A

the boundary between rod and interprismatic enamel

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281
Q

what does the prism sheath contain

A

organic material

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282
Q

what is the prison direction (except from in cervical region)

A

from the EDJ to the surface like spokes of a wheel but with a 3D curve

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283
Q

what is the prism direction in cervical enamel in primary teeth

A

obliquely oriented towards the oral cavity

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284
Q

what is the prism direction in the cervical enamel in permanent teeth

A

obliquely oriented toward the alveolar crest

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285
Q

why is the direction of the rods important in cavity preparation

A

cavity prep must be done in the same direction as the rods

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286
Q

what is prisms decussation

A

bundles of enamel rods cross eachother as they travel from EDJ to the surface

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287
Q

what path do groups of enamel rods follow

A

sinusoidal

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288
Q

what is the benefit of prism decussation

A

it strengthens the enamel structure, prevents propagation of cracks into deeper areas of the enamel, and improves the resistance to fracture

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289
Q

what are Hunter-Schreger Bands

A

an optical phenomenon occurs in the inner two-thirds of enamel, as an alternating light and dark bands

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290
Q

what is the underlying mechanism responsible for Hunter-Schreger Bands

A

prism decussation

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291
Q

what are parazones

A

prism bands that are cut longitudinally (light zones)- reflective zones

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292
Q

what are diazones

A

prism bands that are cut transversely (dark zones)- transparent zones

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293
Q

what is gnarled enamel

A

an area with exaggerated prism decussation (extremely angular) over cusp tips

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294
Q

what causes gnarled enamel

A

the ameloblasts adapt to the rapidly expanding enamel surface and as the crown becomes larger, cohorts of ameloblasts are displaced apically by their own enamel production

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295
Q

where does scalloping occur

A

on the EDJ

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296
Q

what does scalloping do

A

increases the surface area for accommodating more ameloblasts where there is a large difference between EDJ area and crown surfaces area

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297
Q

what is the benefit of a scalloped enamel dentine junction

A

strengthens the attachment of enamel to dentine
prevents the shearing of enamel during function
less scalloped in primary vs permanent

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298
Q

what does prism decussation result in

A

hunter-schreger bands and gnarled enamel

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299
Q

what is the neonatal line

A

an incremental line that occurs at birth resulting from stress

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300
Q

how can the neonatal line be identified

A

its darker than other incremental lines

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301
Q

how does daily enamel secretion rate vary

A

it increases from the EDJ to the enamel surface in both permanent and primary teeth

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302
Q

how many micrometers is the inner, mid and outer enamel in permanent cuspal

A

2-3 inner
3-4 mid
4-5 outer

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303
Q

how many micrometers is the enamel from the EDJ to the surface in lateral primary enamel

A

2.5 to 4.5

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304
Q

by how much do daily enamel secretion rates drop by per day across the neonatal line in primary teeth

A

0.5 microns per day

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305
Q

what are cross striations (short daily lines)

A

DAILY secretion of enamel

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306
Q

how do cross striations form

A

they are the result of a daily variation in ameloblast secretion rate and mineralisation

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307
Q

what are cross striations (short daily lines) equivalent to in dentine

A

von Ebner lines however they are weaklier defined with a closer spacing

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308
Q

what are the Striae of Retzius (long period lines )

A

WEEKLY, wider lines, more defined and result from the ameloblast position at various points of time during development

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309
Q

what are the striae of retzius (long period lines) equivalent to in dentine

A

Anderson lines

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310
Q

how many short period lines are between 2 long period lines

A

7-10

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311
Q

what are accentuated striae

A

neonatal line also produced due to systematic disturbance

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312
Q

what is perikymata

A
  • Perikymata is the outward aspect of internal growth increments
  • Visible on teeth to naked eye
  • The normal transverse wavelike grooves or lines on the external surface of the tooth
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313
Q

what are the enamel incremental growth lines

A

cross striations - short daily lines
striae of retzius- long period lines
perikymata

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314
Q

what do the striae of retzius represent

A

the growth of all the prisms at that increment

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315
Q

what are perikymata surface manifestations of

A

striae of retzius

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316
Q

what are hunter schreger bands related to

A

prism orientation

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317
Q

what are the structural defects of enamel

A

enamel tufts
enamel lamellae
enamel spindles

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318
Q

what are enamel tufts

A

hypomineralised voids following the direction of decussation

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319
Q

where are enamel tufts and what do they contain

A

inner third of enamel, start at the EDJ and project outwards

they contain organic material (mainly tuftelin)

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320
Q

how do enamel tufts appear

A

like lines and only travel for a short distance

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321
Q

what are enamel lamellae

A

when enamel tufts pass through the entire thickness of enamel (contain organic material)

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322
Q

enamel lamellae appear visually as cracks, how are they different

A

cracks are still mineralised enamel where as lamellae enamel is hypomineralised and they contain organic material

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323
Q

what are enamel spindles

A

formed from an odontoblast process embedded into the first zone of enamel, mainly in the cusp tips

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324
Q

why do enamel spindles not follow prism direction

A

Tomes’ process produces enamel at and an angle

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325
Q

what is enamel erosion

A

the chemical dissolution of dental hard tissues from acid that does NOT originate from bacteria (extrinsic or intrinsic acid) , resulting in irreversible tooth surface loss

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326
Q

what is the process by which enamel erosion occurs

A
  1. hydrogen ions dissociate from the acids & interact with the HA crystal causing dissolution (combine with carbonate/phosphate)
  2. this releases all ions from that region of the crystals creating the typical honey comb etched surface
  3. the core of the enamel prisms has been dissolved by the acid and the adjacent interprismatic areas appear more prominent
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327
Q

what is the connective tissue from the dental pulp derived from

A

mesenchymal cells of the dental papilla

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328
Q

what are the 2 types of pulp

A

coronal pulp and radicular pulp

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329
Q

what does the pulp open into through the apical foramen

A

the periodontal ligament

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330
Q

what does the dental pulp provide entry for

A

blood vessels- nourishment
nerves- sensation
lymphatic vessels- lymph drainage

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331
Q

why may there be 3 roots present instead of 2 and what problems can this cause

A

accessory canals present- they are the source of infection and inflammation

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332
Q

what is the dental pulp and whats it made up off

A

loose connective tissue made up of:

  • ECM
  • different cell types
  • blood and lymphatic vessels
  • nerves
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333
Q

what does the dental pulp contain

A

75% water

25% organic material

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334
Q

is there hard tissues in the dental pulp

A

usually no but calcifications and pulp stones can be found in the pulp of aged teeth

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335
Q

what are the histological zones of the dental pulp

A

odontoblast cell layer
cell free zone
cell rich zone
pulp core

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336
Q

where do nerve endings terminate

A

cell free zone

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337
Q

what is the shape and structure of odontoblasts

A

coronal are columnar
cellular processes reaching into the dentinal tubule
cuboidal in root

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338
Q

what happens to the odontoblast layer as the tooth matures

A

it becomes flatter and the number of cells is reduced by apoptosis

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339
Q

what does secondary dentine do

A

its laid at a slower rate after root completion and reduces the size of the space occupied by the dental pulp

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340
Q

how can tertiary dentine be produced

A

in response to external stimuli, odontoblast-like cells can differentiate from progenitor cells in the pulp

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341
Q

what are the types of junctions between odontoblasts

A
  • tight junctions
  • desmosomes
  • gap junctions
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342
Q

what are tight junctions and desmosomes , what is there function

A

mechanical union between 2 cells
maintain spatial relationship
restrict substances in the pulp from entering the dentine

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343
Q

what do gap junctions allow for

A

openings allowing exchange of small molecules and cell-to-cell communication

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344
Q

what are fibroblasts most abundant

A

within the dental pulp (particularly in coronal & cell rich zone)

345
Q

what do fibroblasts produce

A

the collagen fibres and ground substance of the pulp matrix

346
Q

what can fibroblasts also do to collagen

A

degrade collagen (collagen turnover)

347
Q

what are the characteristics of a young pulp

A

large, centrally located nucleus

multiple cellular processes

348
Q

what are the characteristics of an aged pulp

A

smaller, spindle-shaped fibroblasts

fewer organelles

349
Q

what are the cell types in the dental pulp

A

fibroblasts
undifferentiated mesenchymal cells
dental pulp stem cells
immune cells

350
Q

what can undifferentiated mesenchymal cells do

A

differentiate into odontoblast-like cells and fibroblasts

the number reduces with age

351
Q

what can dental pulp stem cells differentiate into

A

Multipotent: odontoblasts, chondrocytes, osteoblasts, adipocytes and neurones depending on the tissue they’re formed in

352
Q

what are the immune cells of the dental pulp

A

macrophages
t and b lymphocytes
neutrophils and eosinophils
dendritic cells

353
Q

what do macrophages do in the dental pulp

A

patrol the pulp and remove dead cells/ bacteria (innate and adaptive immunity)

354
Q

what do neutrophils and eosinophils do in the dental pulp

A

they respond to infection and mediate inflammation

355
Q

what do dendritic cells do in the dental pulp

A

present foreign antigens to T cells

356
Q

what do t and b lymphocytes do in the dental pulp

A

adaptive (antibod-driven) immune system

357
Q

what makes ip the ECM of the dental pulp

A
collagen fibres 
ground substance (non-fibrous protein matrix)
358
Q

what collagen is in the ECM of the pulp and what does it do

A

type I and III (creates meshwork by linking type 1)

forms a scaffold providing stability to the pulp

359
Q

what are the ground substances in the ECM of the pulp

A
  • glycosaminoglycans
  • hydrophilic molecules (swell and form hydrogel that fills most of the extracellular space)
  • growth factors (cellular process regulation)
360
Q

where do the collagen fibres type I and III form

A

as bundles at the roots area not the coronal

361
Q

what is the vascular supply of the pulp

A

blood vessels originating from periodontal ligaments (enter pulp via apical fo)
-peripheral blood vessels branching out towards the odontoblast

362
Q

what controls capillaries

A

nerves

363
Q

what are the lymphatic vessels in the dental pulp involved in

A

the drainage of tissue fluid

364
Q

what is the difference between blood vessels and lymphatic vessels

A

have thinner walls and no red blood cells

365
Q

how many nerve axons enter through the apical foramen

A

2,500 nerve axons

366
Q

what are the types of nerve fibres in the dental pulp

A

myelinated afferent nerve fibres (25%)

unmyelinated C fibres (75%)

367
Q

what are the myelinated afferent nerve fibres and what do they do

A

schwann cells forming the myelin sheath

transmit pain sensation to the CNS; cell bodies in trigeminal ganglion

368
Q

what are the unmyelinated C fibres and what do they do

A

afferent (main) or efferent (minor)

sense changes in extracellular environment

369
Q

what do the afferent unmyelinated fibres do

A

terminate at odontoblast layer or in the dentinal tubules to transmit any noxious stimulus (pain)

370
Q

what do the efferent unmyelinated fibres do

A

terminate on smooth muscle cells of the aterioles to regulate capillary blood flow

371
Q

what is the plexus of raschkow

A

extensive nerve plus that terminates in the cell-free zone, just below the odontoblast layer of the crown
(axons can pass between odontoblasts & enter dentinal tubules)

372
Q

where is the nerve plexus

A

coronal, not in root canals

373
Q

what is the main function of the dental pulp

A

provide vitality to the tooth and nourishment of odontoblasts via blood vessels/capillaries

374
Q

how does the dental pulp have a protective function

A
  • sensation of external stimuli via nerves and their endings
  • barrier/defence- tertiary dentine triggering an inflammatory response
375
Q

what are the clinical issues with the pulp

A
age changes
infection spread and inflammation 
RCT 
calcifications and pulp stones
dentine sensitivity
376
Q

what is the challenge associated with a young tooth

A

large pulp chamber so challenge for cavity/crown preparation (thin dentine layer and pulp exposure can easily occur)

377
Q

what is the challenge associated with an old tooth

A

narrow pulp chamber and narrow root canal so challenge for RCT, secondary dentine also accumulates

378
Q

how can caries spread

A

from the dental pulp into the surrounding periodontal tissues (abcess)

379
Q

how can periodontal disease spread

A

from the surrounding periodontal tissues into the dental pulp e.g. through accessory root canal

380
Q

what do calcifications and pulp stones form in response to

A

a chronic stimulus (e.g. caries infection or as an age related change

381
Q

why does an older pulp form calcifications and pulp stones

A

less vascular

382
Q

what can false pulp stones be formed from

A

calcifying blood vessels and contain bone-like material (inflammation then healing)

383
Q

what are true pulp stones formed from

A

detached odontoblasts and contain dentine

384
Q

how does dentine sensitivity occur

A

afferent nerve endings terminating in the dentine or near odontoblasts sense pain, mechanical, thermal and tactile stimulus

385
Q

what are the 3 theories for dentine sensitivity

A
  • neural theory- dentine directly innervated
  • odontoblasts act as receptors
  • hydrodynamic theory- fluid movement in dentinal tubules is sensed directly/indirectly by nerve endings
386
Q

when is HERs formed in root formation

A

after the formation of the crown

387
Q

how is HERs formed

A

epithelial cells of the IEE and OEE initially proliferate downwards from the cervical loop of the enamel organ to form a double layer of epithelial cells

388
Q

what does HERs define when it extends around the pulp

A

the shape of the future root

389
Q

what is the difference of HERs to the cervical loop

A

there is no stratum intermedium and no stellate reticulum

epithelial: PTHrP and enamel proteins
mesenchymal: TGF-β, BMP, RUNX2 (cementoblast differentiation and periodontal regeneration)

390
Q

how is odontoblast differentiation initiated in the root

A

the IEE of HERS induces it

391
Q

what is the difference between odontoblast induction at HERS in the root over the differentiation at the cervical loop

A

no ameloblast differentiation in root
predentine secreted which forms dentine
primary apical fo forms
HERS becomes stretched

392
Q

what term is used to describe the curved end of HERS that outlines the primary apical fo

A

epithelial diaphragm

393
Q

what is the role of HERS in tooth eruption

A

cell proliferation of epithelial cells- its position remains stationary and the dentine at the bottom moves the tooth upwards

394
Q

why was the growth displacement theory disproved

A

teeth can still erupt of the root is blocked

395
Q

how are the PDL involved in tooth eruption

A

rearrangement of collagen fibres and contraction, tooth is pulled up and the bone is removed to create the space

396
Q

what are the layers of root dentine

A

cementum
hyaline layer
tome’s granular layer
root dentine

397
Q

what are the two explanations of Tome’s granular layer

A
  • extensive branching and backwards looping of odontoblasts processes
  • incomplete fusion of calcospherites (similar to interglobular dentine)
398
Q

what are the differences of root dentine compared to coronal dentine

A
  • collagen fibres are deposited parallel and at a distance from the basal lamina of HERS
  • root dentine is less mineralised and mineralises faster
  • less phosphophoryn
399
Q

what is phosphophoryn

A

dentine phosphoprotein- it binds calcium and regulates dentine mineralisation

400
Q

how does HERS enclose the pulp and appear

A

as a ‘curtain’ hanging from the crown

401
Q

how does the primary apical foramen divide

A

by the fusion of epithelial folds from HERS

402
Q

at eruption the roots is only at what percentage of its final length

A

roughly 65%

wide open root apex

403
Q

when does the root complete for primary and permanent teeth

A

1.5 years after eruption for primary

3 years after eruption for permanent

404
Q

cementoblasts differentiate from what cells

A

undifferentiated mesenchymal cells of the dental follicle

405
Q

what occurs before the differentiation of dental follicle cells occur

A

odontoblast induction from dentine formation

stretching and disintegration of HERS

406
Q

what do dental follicle cells differentiate into

A

osteoblasts (alveolar bone)
fibroblasts (PDL)
cementoblasts (cementum)

407
Q

what are the two theories of cementoblast differentiation

A

inductive signals from gaps in disintegrating HERS/predentine sent to undifferentiated dental follicle cells
epithelial-mesenchymal transmission (EMT) of HERS to cementoblasts

408
Q

is cementum vascular or avascualr

A

avascular

409
Q

what is the function of cementum

A

attachment of root dentine to PDL

410
Q

what is the % of hydroxyapatite in cementum

A

40-50%

411
Q

what is the benefit of the hydroxyapatite in cementum

A

allows the resistance to root resorption

412
Q

what are the types of collagens in cementum

A

type I- 90%
type III
type XII

413
Q

what are the non -collagens in cementum

A

alkaline phosphotase, bone sialoprotein, dentine matrix protein matrix protein 1, dentine sialoprotein, osteocalcin, osteonectin, osteopontin

414
Q

what do you classify cementum according to

A

the absence or presence of cells : acellular (primary) or cellular (secondary)
the origin of collagen fibres in cementum : extrinsic or intrinsic

415
Q

how is cementum distributed in most people at the cementoenamel junction

A

cementum overlaps enamel- 60%
cementum meets enamel - 30&
cementum and enamel dont meet - 10%

416
Q

where is acellular cementum found

A

covering the root adjacent to dentine (primary attachment)

417
Q

where is cellular cementum found

A

in apical and interradicular (in between roots)

418
Q

what is the function of cellular cementum

A

adaption and repair

thickeness increases with age

419
Q

what are the cells in cellular cementum

A

lacunae and canaliculi containing cementocytes and their processes

420
Q

in which cementum is the development relatively fast

A

cellular

421
Q

in which direction are the calnaliculi directed

A

towards the PDL

422
Q

where do cementoblasts align in the early formation of accellular cementum

A

along newly formed hyaline layer

423
Q

what is the fibrous fringe

A

extension of cementoblast cell process into predentine and deposition of collagen fibres that intermingle with un-mineralised predentine matrix

424
Q

how do the PDL stitch to the fibrous fringe

A

by the extension of collagen fibres

425
Q

how do collagen fibres become trapped in predentine causing strong connection of cementum to dentine

A

it mineralises and spreads through the cementum

426
Q

what are the incremental growth lines in cementum

A

lines of salter

427
Q

what are cementicles and where do they sit

A

a group of cementoblast that become detached

in PDL

428
Q

what are the epithelial rests of malassez

A

clusters of epithelial cells on PDL (potentially regenerate periodontal tissue) that have been left behind during the apoptosis of HERS

429
Q

where do enamel pearls occur

A

where the root bifurcates (of maxillary molars)

430
Q

how can enamel pearls cause plaque accumulation and PD

A

the distrust of attachment of the tooth creates an entry point for bacteria

431
Q

what are the mechanisms of enamel pearl formation (hypothesises)

A
  • attachment of Epithelial Cell Rests (ECR) to predentine (caused by absence of cementum deposition) which may receive signals from predentine and initiate ameloblast differentiation
  • stellate reticulum and stratum intermedium cells of the cervical loop become trapped in a subset of ECRs when HERS/rot development is initiated
432
Q

why does there need to be combination of hypothesises for the development of enamel pearls

A

you need to the molecular signals from the pre-dentine for but you need the relevant cells that support ameloblast differentiation

433
Q

what are the clinical considerations during root development

A

concrescence
dilacerated roots
roots and canals multiple
hypercementosis

434
Q

what is concresence

A

union of two teeth after eruption resulting from a fusion of their cementum surfaces

435
Q

what are the causes of concresence

A

trauma and tooth crowding

436
Q

what are the clinical considerations for concresence

A

radiography and surgery

437
Q

what are dilacerated roots (causes and clinical considerations)

A

curved or bent roots
caused by developmental trauma (playground accidents)
CC: radiographs and careful extraction

438
Q

how do multiple roots or root canals form

A

abnormal folding of HERS

439
Q

what are the clinical considerations when there are multiple roots or root canals formed

A

radiograph and variation of extraction technique

careful cleaning of extra root canal during endodontic treatment

440
Q

what is the difference between a lateral and accessory root canal

A

lateral - connections between root canals

accessory - form in the apical foramen

441
Q

what is the mechanisms of lateral root canal formation

A

continuity of HERS is interrupted too early during root dentin formation
this affects local formation odontoblasts resulting in a canal in the dentine connecting the dental pulp and the PDL of the mature tooth

442
Q

what is hypercementosis

A

abnormal production of cellular cementum (produced after the root is completely developed)

443
Q

what are the causes of hypercementosis

A
age change 
paget's disease 
idiopathic 
occlusal trauma 
patients that grind their teeth - tooth moves up so space is filled with cementum
444
Q

what are the clinical considerations for hypercementosis

A

increased distance from CE junction to root apex (imp in endodontic treatment)

445
Q

how does coordinated root and periodontal tissue formation occur

A

odontoblast induction and dentine formation
stretching and disintegration of HERS
differentiation of dental follicle cells

446
Q

what do dental follicle cells differentiate into

A

cementoblast (cementum)
fibroblasts (PDL)
osteoblasts (alveolar bone)

447
Q

what are FGFs thought to regulate

A

cell proliferation and migration in the formation of periodontal tissue

448
Q

what are BMPs thought to regulate

A

cell differentiation and bone formation in the formation of periodontal tissue

449
Q

what growth factors stimulate periodontal regeneration

A

FGF2, BMP2

450
Q

what are stem cells in PDL a source of

A

regenerative therapies in periodontal disease e.g. mesenchymal cells

451
Q

what are the functions of the PDL

A
  • tooth attachment
  • withstand forces of mastication
  • sensory receptor
  • remodelling function
  • nutritive function
452
Q

how does PDL aid tooth attachment

A

PDL fibres insert into cementum and alveolar bone to form fibrous joint with little/no movement (gomphosis, synarthrosis)

453
Q

how does PDL act as a sensory receptor

A

sensation of pain and tension/compression

repositioning of teeth to achieve occlusion

454
Q

how does the PDL have a remodelling function (tooth movement)

A

high turnover of extracellular matrix and collagen fibres (source of progenitor/stem cells)

455
Q

how does the PDL have a nutritive function

A

high vascularised tissue; connected to dental arteries, bone marrow and gingiva. blood vessels needed to perform remodelling function

456
Q

how does timing of PDL development and differentiation vary

A

among species
between tooth types
between primary and permanent teeth

457
Q

what is involved in the initiation stage of PDL development

A
  • ligament space between cementum and bone consists of an unorganised connective tissue (fibroblasts and ecm)
  • short fibre bundles are formed near cementum and bone and extend a short distance into the ligament space
458
Q

how do fibre bundles gradually extend from bone to cementum in PDL formation

A

fibroblasts produce more collagen fibrils that assemble as fibre bundles

459
Q

how does the thickness of fibres bundles vary from the bone side and cementum side

A

bone side: thick fibre bundles

cementum side: thin fibre bundles

460
Q

where are alveolar crest fibres first formed

A

at cemento-enamel junction (fibres form apically as the root forms)

461
Q

what orientation are the alveolar crest fibres

A

initially oblique, then parallel, then oblique

462
Q

when do thick alveolar fibre bundles only form

A

when teeth occlude and function - this is bc mechanical sensation induces the completion of PDL development

463
Q

what are the principle fibre groups of the PDL

A
alveolar crest group
horizontal group 
oblique group 
apical group 
apical group
interradicular group
464
Q

where is the alveolar crest group and whats it function

A

below CEJ- rim of alveolus

resists extrusive forces (must overcome when extracting the tooth)

465
Q

where is the horizontal group and what is its function

A

below the alveolar crest group, at right angles to tooth axis

resists horizontal forces (tipping)

466
Q

what is the function of the oblique group

A

resists intrusive (‘compressive’) forces - mastication

467
Q

where is the apical group and whats its function

A

radiates around tooth apex

resists intrusive forces

468
Q

where is the interradicular group and whats its functiojn

A

connects to crest of interradicular septum; only in mutli-rooted teeth

resists extrusive forces- overcome when extracting tooth

469
Q

what are the principle fibre groups of the PDL that need to be overcome when extracting a tooth

A

alveolar crest group

interradicular group

470
Q

what are the elastic fibres of the PDL and where do they run

A

oxytalan fibres and fibrillin (no elastin)

run perpendicular to collagen fibres in cervical region

471
Q

what is the function of elastic fibres

A

associated with neurovascular bundles; form 3D meshwork surrounding root and REGULATE vascular flow

472
Q

what is the function of sharpey’s fibres

A

mineralised PDL fibres in alveolar bone and cementum

473
Q

what are the cell types in the PDL

A
fibroblasts
osteoblasts and osteoclasts 
cementoblasts and cementoclasts
rests of malassez
immune cells 
blood vessels
nerve fibres
474
Q

what is the function of fibroblasts in the PDL

A

produce collagen fibres, growth factors and ground substances (ecm)
perivascular and endosteal fibroblasts surround the blood vessels

475
Q

what is the collagen half life

A

3-23 days (highest turnover at tooth apex)

476
Q

what cell to cell contacts do fibroblasts in the PDL form

A

adherens junctions and gap junctions

477
Q

how is the activity of fibroblasts in the PDL induced

A

by mechanical/masticatory forces

478
Q

how do fibroblasts have a dual function in remodelling in the PDL

A

synthesis and degradation of ECM and collagen; matrix metalloproteases

479
Q

why are matrix metalloproteases (MMPs) the therapeutic target in periodontal disease

A

they’re the enzyme involved in collagen turnover and are highly active periodontal disease

480
Q

what is the composition of the PDL

A

60% ground substance (mainly collagen fibres, blood vessels and nerves)
fibres: 90% collagen, 10% oxytalan(microfibrils without elastin)
collagen types: I(80%), III(15%), IV, V, VI, VII, XII

481
Q

when are type XII collagen fibres present and what is there function

A

usually not during development , only after eruption

fibril-associated: link other collagens. expressed on pressure side following mechanical loading

482
Q

what is the ground substance in the PDL composed of

A

complex composition of glycosaminoglycans: hyaluronic acid, dermatan surface, chondroitin and heparin sulfate) ,proteoglycans and glycoproteins

483
Q

what is the function of the ground substance

A

ion and water binding
70% shock absorber
orientation of collagen fibres

484
Q

what does the ECM control

A

the hydration of the tissues and increases the strength of collagen fibrils

485
Q

how does the composition of the ground substance vary according to developmental state

A

hyaluronan decreases during development of PDL from dental follicle
proteoglycans increase during tooth development

486
Q

what does the fibronectin in ground substance do

A

mediates attachment of cells to collagen fibrils - influence on cell migration and differentiation
clinically promotes wound healing

487
Q

what growth factors and cytokines does he ECM bind in the ground substance

A
FGF
TGF-beta (BMP)
IGF
PDGF
VEGF
interleukins
prostaglandins
488
Q

what is the function of the rests of malassez in the PDL

A

they’re remnants of HERS and a source of all mesenchymal cell types e.g. fibroblasts, osteoblasts, cementoblasts

489
Q

what are the immune cells of the PDL

A

macrophages
mast cells
eosinophils

490
Q

how does the vascularisation of the PDL vary

A

between species, tooth types, erupting teeth

491
Q

what arteries supply the PDL

A

branches of superior and inferior alveolar arteries

branches of the lingual and palatine arteries entering through the gingiva supplying the PDL

492
Q

how do the superior and inferior alveolar arteries enter the PDL

A

enter the pulp at apex
interalveolar vessels pass through the alveolar process (perforating arteries)

more abundant in posterior and mandibular teeth to supply PDL

493
Q

what do the interalveolar vessels do

A

form interstitial areas
enable PDL function after endodontic treatment- nutrients needed through interalveolar vessels
extractions wounds: formation of blood clot and invasion of cells involved in healing

494
Q

what are neurovascular bundles in PDL

A

pass through perforations in the alveolar bone and form the interstitial areas in the PDL - contain blood vessels and nerves

495
Q

where are interstitial areas in the PDL usually located

A

closer to the alveolar bone

496
Q

where do blood vessels form a capillary plexus in PDL

A

near the root surface and a postcapillary plexus from which venules pass into the alveolar bone

497
Q

what directions do blood vessels run in

A

apical occlusal direction and form arteriovenous anastomoses

498
Q

where does venous drainage in the PDL occur

A

at apex, removal of waste products

499
Q

what does the circular plexus surround

A

the root surface

500
Q

what does the crevicular plexus surround

A

the tooth in the region beneath the gingival crevice

501
Q

what are fenestrated capillaries

A

pores in endothelial cells that surround blood vessels - special feature of the PDL and not seen in other connective tissue

502
Q

what do fenestrated capillaries do

A

increase diffusion capacity which is consistent with the high metabolic rate in the PDL (esp during tooth eruption)

503
Q

how is PDL innervation distributed

A

follows pattern of vasculature

perforating nerve fibres divide into an apical and gingival branch

504
Q

what is the regional variation for PDL innervation

A

more nerve endings at the tooth apex
upper incisors have denser innervation throughout the PDL compared to molars
related to masticatory response

505
Q

what are the types of nerve fibres in the PDL

A

sensory - nociception and proprioception
autonomic - blood flow regulation
myelinated- sensory only
myelinated and unmyelinated- sensory and autonomic

506
Q

what are the types of nerve endings in the PDL

A

free-ending, tree like
ruffini’s corpuscles
coiled type
encapsualted spindle type

507
Q

where are free nerve endings and what is there function

A

-Evenly distributed across the PDL
Unmyelinated fibres (enveloped by one Schwann cell; inset)
Extend up to the cementoblast layer
Sense pain and pressure

508
Q

where are ruffuni’s corpuscles and where are they found

A

in PDL at root apex
myelinated fibres with dendritic endings
associate with collagen fibres
sense pressure

509
Q

where are coiled nerve endings found

A

middle of PDL

510
Q

where are encapsulated spindles found

A

in PDL at root apex

surrounded by fibrous capsule

511
Q

what is the general thickness of the PDL

A

0.15-0.38mm thinnest in middle of root

512
Q

what is the PDL thickness for 11-16 years

A

0.21mm

513
Q

what is the PDL thickness for 32-52 years

A

0.18mm

514
Q

what is the PDL thickness for 53-67 years

A

0.15mm

515
Q

what does mastication induce

A

periodontal remodelling increasing PDL width by 50% including thicker fibre bundles and increased alveolar bone size

516
Q

where is PDL thicker

A

in areas are tension rather that compression

517
Q

what results in periodntal tissue loss

A

reduced function

518
Q

how does Capacity for PDL remodelling form the basis for orthodontic treatment

A

Excessive force can cause localised necrosis of the PDL by cutting off the normal bloody supply to the cells. E.g. too much pressure

519
Q

how can Damaged PDL be repaired from cells in vital parts

A

Failure of repair causes localised resorption and tooth ankylosis (fusion of tooth to alveolar bone;)  problem extracting

520
Q

how can Accidentally lost teeth can be replanted

A
  • If portions of the ligament are permanently damaged, external root resorption and ankylosis could occur. Progenitor cells in the PDL can restart the process and reintegrate the toot into the socket
521
Q

why is PDL is a target of therapies for periodontal disease

A
  • Prevention of undesirable wound healing (guided tissue regeneration – prevent undesired wound healing in PD treatment)
  • Growth factors, cytokines or stem cells to stimulate PDL regeneration
522
Q

what forms of the tooth sockets

A

the alveolar process of the mandible

523
Q

what are 3 mechanisms of bone formation

A

endochondral ossification
intramembranous ossification
sutural ossification

524
Q

what is involved in endochondral ossification

A

bone made from a cartilage model - chondrocytes produce cartilage that is replaced by osteoid/bone produced by osteoblasts

525
Q

what are examples of bone produced by endochondral ossification

A
long bones(epiphyseal growth plate),
base of skull (synchondrosis)
mandibular condoyle (secondary cartilage)
526
Q

what is involved in intramembranous ossification

A

bones are made by osteoblasts that have differentiated from mesenchymal stem cells and lay down the bone directly
it is determined by the spaces around where the bone forms

527
Q

what are examples of bones produced by intramembranous ossification

A

flat skull bones

facial bones: mandible, maxilla and alveolar bone

528
Q

what is involved in sutural ossification

A

similar to intramembranous o. but with fibrous connection

provides stability during growth

529
Q

what are examples of bone enabled by sutural ossification

A

postnatal growth of flat skull bones

530
Q

what makes up bone composition

A

mineralised living connective tissue

non-collagenous proteins

531
Q

what is mineralised living connective tissue

A

organic matrix is permeated by hydroxyapatite (deposited between type I collagen fibrils)

532
Q

what are non-collagenous proteins and what is their fucntion

A

bone sialoprotein, osteocalcin, osteonectin, osteopontin (all of these bind to ca or HA)

control of mineralisation, proteoglycans, cytokines, growth factors, serum proteins

533
Q

what is the main function of bone

A

support, protection, locomotion, mineral reservoir

534
Q

what hormones is bone physiology controlled by

A
(-)PTH
(+)Calcitonin 
(+)Vitamin D
(+)Estrogen (decreased after menopause)
(+)Leptin
535
Q

what growth factors and cytokines does bone secrete

A

GF: BMP, TGF-ß, PDGF, IGF
Cytokines: Interleukins, TNF, RANKL

(bone also secretes neuroendocrine factors)

536
Q

what is meant by ‘woven’ bone

A

bone formed during development characterised by randomly orientated collagen fibrils. it becomes replaces by lamellar bone

537
Q

when else is ‘woven’ bone formed except from during development

A

bone fracture repair

- forms as part of the wound healing response but eventually replaced by lamellar bone

538
Q

what is adult bone composed of

A

compact (denser outer area) and trabecular bone (cancellous, spongy)

539
Q

what is trabecular bone

A

cavity filled with bone marrow interrupted by a network of bone plates (trabeculae), leaving spaces in between where the bone marrow sits

540
Q

what are examples of adult bone

A

mandible

long bones

541
Q

what are bone lamellae

A

different types of bone layers

542
Q

what are the 3 types of bone lamellae

A

circumferrrential lamellae
concentric (Haversian) lamellae
Interstitial lamellae

543
Q

what is circumferrential lamellae

A

encloses the entire outer and inner perimeter of the bone

544
Q

what is concentric lamellae

A

forms the basic unit bone (osteon) and makes up the bulk of the compact bone

545
Q

what is interstitial lamellae

A

interspersed between adjacent osteons (remnants of remodelled osteons

546
Q

are osteons transient or static

A

they’re transient so are constantly resorbed and formed

547
Q

wha are osteons

A

cyclinder of bone (generally parallel to the long axis of he bone)

548
Q

what is the osteon composed of

A
central canal (haversian canal) including a blood capillary lined by a layer of osteoblasts
volkmann's canals - interconnect adjacent central canals
549
Q

how can osteblasts remodel osteons from inside

A

they can enter through blood vessels

550
Q

what is the periosteum

A

connective tissue membrane consisting of two layers

551
Q

what are the two layers of the periosteum and what are they composed of

A

outer fibrous layer- dense collagen fibres

inner cellular layer- osteoblasts and their precursors, highly vascularised

552
Q

what is the endosteum and what is its composition

A

the internal surface
not well demarcated, loose connective tissue including osteoblasts; separates bone surface from marrow; less active in bone formation than periosteum

553
Q

what are the bone cells

A

osteoblasts
osteocytes
osteoclasts

554
Q

what are the characteristics of osteoblasts

A

cuboidal cell shape

inactive: flat, bone lining cells

555
Q

where are osteoblasts derived from and what do they synthesise

A

mesenchymal stem cells

synthesise organic bone matrix

556
Q

what do osteoblasts produce

A

osteoid (mainly collagen type I)
alkaline phosphatase- cleaves inorganic phosphate to initiate and promote mineralisation
growth factors- : IGF1, TGF-ß, PDGF which increase bone repair (dental therapy - implants)

557
Q

what are osteocytes

A

osteoblasts that become trapped in unmineralised or mineralised matrix

558
Q

what is a lacunae and how is it produced

A

spaces in the matrix produced by

osteocytes becoming smaller in size

559
Q

what are canaliculi and how do they form

A

canals between lacunae

formed from a network of cellular processes that connect adjacent osteocytes

560
Q

what do osteocytes function as

A

sensors of changes in the bone environment

signalling centres to maintain bone integrity (induce bone remodelling)

561
Q

what are osteoclasts

A

large multinucleated cells; derived from haematopoietic cells

562
Q

what do osteoblasts produce

A

Howship’s lacunae (resorption bays -holes in bone)

acid phosphates and lysosomal enzymes

563
Q

what occurs in the resorption sequence

A
  • attachment of osteoclasts to bone
  • creation of acidic microenvironment for demineralisation
  • degradation of exposed matrix by enzymes
  • endocytosis of degradation products
564
Q

what occurs in intramembranous ossification

A

mesenchymal cells in the cellular periosteum differentiate to become osteoblasts which produce woven bone (irregular)

gradual turnover/remodelling of woven bone to lamellar bone - formation of primary osteon

continued bone replacement produces highly organised mature bone with fewer cells, secondary and tertiary osteons and circumferential lamellae

565
Q

what does the mature bone space consist of

A

mineralised bones and very few osteocytes

566
Q

outline the development of the alveolar process

A

mandible takes the shape of a trough underneath the inf. alveolar nerve. the alveolar process begins to grow towards the tooth germ and will start surrounding it

alveolar process almost surround the incisor tooth germ. the inferior alveolar nerve is enclosed in a bony canal

to accommodate the growing tooth germ, the alveolar bone must be resorbed on the inner wall of the alveolus and new bone must be deposited on the outer wall

567
Q

what cells are involved in bone remodelling

A

osteoblasts- area of bone formation
osteoclasts- area of bone resorption (lacunae)
osteocytes- osteoblasts embedded in bone
bone lining cells- flat area of no bone activity

568
Q

what is the function of bone lining cells

A

protection from resorption by osteoclasts
initiating bone remodelling
mineral metabolism
source of progenitor cells

569
Q

what are the stage of bone remodelling

A

resorption- osteoclasts
reversal- cessation of resorption, disappearance of osteoclasts
formation- recruitment, migration and differentiation of osteoblasts (bone formation)
resting- bone in tact but remodelled, cessation of bone formation, surface covered by flat bone-lining cells

570
Q

what are the structural lines in bones

A

resting lines- pause in bone deposition, osteoblasts stop producing bone- parallel

reversal lines- change from bone resorption to deposition (position of howships lacunae)- scalloped

571
Q

what is involved in the life cycle of an osteon

A

resting
formation
reversal
resorption

572
Q

what are the components of the tooth socket

A
buccal cortical plate
lingual cortical plate 
cribiform perforations in bone for blood vessels and nerves to enter PDL 
interdental septum (between teeth) 
interradicular septum (between roots)
573
Q

what is the structure of alveolar bone

A
  • outer compact layer: cortical plate
  • central trabecular layer: spongiosa
  • inner compact layer: alveolar plate, perforated to allow access to blood vessels connecting PDL
  • alveolar crest (1.5-2mm below CEJ)
574
Q

what is the cortical plate- where is it thickest and thinnest

A

surface layer of lamellar bone supported by osteons
thinner in maxilla than mandible
thickest on buccal aspect of mandibular premolars and molars

575
Q

what is spongisa composed of

A

trabecular (cancellous) bone

-bone marrow spaces rich in adipose tissue which is an energy storage

576
Q

where is spongisa absent

A

in anterior teeth; cortical and alveolar plate fused

577
Q

what is the alveolar plate composed of

A

lamellar bone and bundle bone

- contains sharpeys fibres

578
Q

what is bundle bone

A

The innermost layer of the alveolar plate (directly lining the socket) is referred to as bundle bone because the collagen fibre bundles of the PDL are embedded

579
Q

what is the function of bundle bone

A

Provides the attachment for PDL fibres

Where fibres are inserted is bundle bone

580
Q

how does remodelling: tooth drift (to the right) occur in orthodontic treatment

A

Resorption by osteoclasts on the right side of the alveolar plate creates the space that the tooth can move into

To compensate for this bone loss new bone must be formed onto the cortical plate on the opposite side. Keeps thickness constant

Because the tooth moves to the right, the space in the socket on the left must be filled by bone deposition onto the alveolar plate

The excess bone must then be resorbed by osteoclasts from the cortical plate on the opposite side

581
Q

through what stage does alveolar bone remodelling procees

A

resorption, formation, resting

582
Q

what is mesial drift

A
  • Unworn teeth have very few interproximal contact points
  • Attrition cause hard tissue loss on occlusal and interproximal surfaces
  • Increase in interproximal distance is compensated by mesial (forward) drift of teeth to fill the gap
  • Broader interproximal contact points
583
Q

what is intraocclusion

A

During trauma or infection can cause tooth ankylosis (fusion of tooth root to alveolar bone ) toot cannot move anymore, can no longer erupt and exfoliate

Most common in primary molars e.g. partial root resorption

584
Q

what are the consequences of intraocclusion and what should be done

A
  • Prevents exfoliation; leads to impaction of successor tooth
  • Further growth of alveolar bone results in “submergence” of ankylosed tooth
  • Extraction to prevent malocclusion or periodontal problems
585
Q

what is lamina dura (clinical consideration)

A

alveolar plate on the dental radiograph is lamina dura

An interrupted lamina dura in the apical region indicates a periapical abscess.

586
Q

what is alveolar bone resorption and when does this occur. what are the consequences of this

A

Following tooth extraction or chronic periodontitis, the alveolar process can resorb:

  • Placement of dental implants will be difficult
  • Implanting soon after tooth loss decreases the rate of alveolar ridge resorption. Should not but implant soon after bone resorbed
  • Bone loss impacts on construction of removable prostheses
587
Q

what is maxillary sinus perforation

A

the Close proximity of premolar/molar roots and alveolar bone to maxillary sinus flow means
During tooth extraction, maxillary floor can rupture (bone can fracture) (oro-antral connection/fistula; infection)

588
Q

what is alveolar osteitis and what does it lead to

A

After tooth extraction, socket fills with blood and forms blood clot: Important step in wound healing- detachment of blood clot and it falls out- ‘dry socket’.
leads to painful bone inflammation and bad odour

589
Q

what is the gingiva

A

the part of the oral mucosa that surrounds and is attached to teeth and alveolar bone - continuum with the oral mucosa or pdl

590
Q

what creates the dentogingival junction and how

A

tooth eruption

during eruption the REE fuses with the oral epithelium

591
Q

what cell type is the REE

A

simple epithelium: cuboidal cells

592
Q

what cell type is the OE

A

stratified squamous

593
Q

what happens when the REE fuses with the OE during tooth eruption

A

degeneration of central epithelial cells, this causes a continuum between the 2 epithelia which prevents the tooth from creating a wound

594
Q

why is there no bleeding when the tooth erupts

A

there is epithelial continuity at all times between REE and OE which means there is no connective tissue exposure. if there is blood it is the remaining blood from the tooth pulp

595
Q

what epithelium is formed when the tooth erupts and the DGJ is formed

A

junctional epithelium (JE)

596
Q

what does the JE consist of, whats its function and is it keratinised or non keratinised

A

entirely REE
attaches gingiva to tooth
it is non-keratinised

JE is very simple and primitive

597
Q

what occurs to the gingiva some time after tooth eruption

A

gingival epitehlium appears to overgrow and replaces the REE

sulcular epithelium occurs

598
Q

what types of epithelium are at the gingival sulcus

A

Junctional epithelium
Sulcular epithelium
Gingival epithelium

599
Q

what cell type is the junctional epithelium

A

simple, non keratinised

600
Q

what cell type is the sulcular epithelium

A

stratified, non keratinised

601
Q

what cell type is the gingival epithelium

A

stratified keratinised

602
Q

what is the mechanism for epitehial change some time after tooth eruption

A

gingival cells change to sulcular which is non keratinised

stratification of early REE and rete peg formation

603
Q

how is the development (depth) of the sulcus induced

A

by masticatory forces acting on the gingiva

base of the sulcus at the same level as free gingival groove, deeper in disease tooth

604
Q

why does the junctional epithelium still appear like REE

A

JE is simple non keratinised and REE is simple cuboidal - very primitive

605
Q

what occurs in the epithelia 2-3 years after tooth eruption

A

the gingival epithelium appears to have completely replaced the REE
small epithelial tag remains from the REE (cell remnants and primary enamel cuticle)

606
Q

what is the primary enamel cuticle (nasmyths membrane)

A

internal basal lamina that the epithelial cells sit, it covers the tooth once erupted but usually worn away by mastication

607
Q

what indicates that junctional epithelial cells are different from gingival epithelial cells

A

molecular markers

REE could become stratified and develop rete pegs

608
Q

what is evidence that stem cells can form JE

A

tooth attachment is restored after gingi-vectomy

gingival tissue grafting possible

609
Q

what 2 enamel matrix proteins are stained in immunohistochemical staining

A

amelotin (AMTN; A)

odontogenic ameloblast-associated (ODAM:B)

610
Q

where is ameolotinn expressed

A

in the basal lamina

normally expressed by the maturation stage ameloblasts forming the REE

611
Q

where is ODAM expressed

A

in internal basal lamina and junctional epithelial cells

612
Q

where is junctional epithelium derived from

A

REE

its not a downgrowth of the gingiva

613
Q

what secretes primary enamel cuticle and what does it do

A

epithelial cells secrete it onto the enamel surface where it bonds with enamel proteins

614
Q

what is a hemidesmosome

A

half a desmosome by which cells below the internal lamina attach

615
Q

what does the external basal lamina attach to

A

lamina propria

616
Q

why is the junctional epithelium permeable and what does the allow

A

there reduced number of desmosomes and larger intracellular spaces

allows the passage of GCF and defence cells into the sulcus

617
Q

what does the GCF contains

A

antibodies
complement factors
macrophages (phagocytes)
desquamated sulcular and junctional epithelial cells (5-6 days turnover)
cytokines and metalloproteases (during infection)

618
Q

what is the function of the GCF

A

inflammatory exudate which is secreted to cleanse out the gingival crevice
first line of defence against bacteria

619
Q

what happens if GCF is overproduced

A

provide subgingival bacteria with excess nutrients potentially allowing harmful bacteria to survive

tissue destruction caused by inflammation

GCF can be an indicator of periodontal health

620
Q

what are the features of attached gingiva

A

alveolar mucosa

submucosa

621
Q

what are the features of free gingiva

A
free gingival groove(border between free and attached)
gingival margin
gingival sulcus 
junctional epithelium 
sulcular epithelium
622
Q

what is the mucogingival junction

A

boundary between the alveolar mucosa and attached gingiva

623
Q

what are the cells of the masticatory mucosa like

A

parakeratinised (and partially orthokeratinised)

624
Q

what are the layers of the gingiva

A

epithelium
lamina propria
mucoperiosteum (submucosa absent

625
Q

what are the features of teh epithelium of the gingiva

A

thick
parakeratinised- live cells in keratin layers

can also be orthokeratinised which occurs when there is a strong masticatory force on gingiva (appears white)

626
Q

what are the features of the lamina propria

A

fibres attach with underlying alveolar bone
long, narrow papillae
dense collagen fibres- makes tissue tough to resist masticatory forces

627
Q

what is the function of the mucoperiosteum

A

stability

submucosa acts as a cushion

628
Q

what is the clinical relevance of the mucoperiosteum

A

difficult to inject and painful for patients

doesn’t require suturing

629
Q

why is the mucoperiosteum present in gingiva instead of submucosa

A

submucosa provides mobility- acts as a cushion e.g in lining mucosa . contains loose connective tissue and salivary glands or adipose tissue.

however in order to withstand masticatory forces the lamina propria is directly joined with the periosteum of bone in e.g. masticatory mucosa to provide stability

630
Q

where do the transseptal fibre groups run and what is their function

A

interdentally from CEJ over the alveolar crest to the CEJ of neighbouring tooth

controls mesio-distal spacing

631
Q

what is the clinical relevance of the transseptal fibre group

A

when braces come off, teeth move back into their original position due to these fibres

632
Q

what does the dentogingival fibre group do

A

(largest group)

connects cervical cementum to lamina propria of free and attached gingiva

633
Q

what does the alveogingival fibre group do

A

connects the alveolar bone crest to lamina propria of free and attached gingiva

634
Q

what does the dentoperiosteal group do and where does it run

A

runs from the cementum over the outer surface of the alveolar process and insert either into the alveolar process or the vestibular muscle and floor of the mouth

635
Q

what does the circular group do

A

(smallest group)
forms bands around the neck of the teeth and interlaces with other fibres in the free gingiva. binds free gingiva to the tooth

636
Q

which gingival fibre is in the gingiva and has the same structure as the junctional epithelium

A

denal col- depression

doesnt attach to any teeth

637
Q

what occurs when mild periodontal inflammation causes gingivitis

A

the inflammatory response in connective tissue attracts immune cells- 70% of collagne fibres are destroyed by this. as a response the sulcular epithelium grows downwards to comepensate for the loss of connective tissue here

638
Q

how do the sulcular and gingival epithelial tissue appear when connective tissue is inflamed

A

deep in growth of both epithelium

639
Q

what occurs if there is persistent inflammation

A

further destruction of connective tissue by inflammatory cells causes apical migration of junctional epithelium- forming a gingival pocket
if advanced: loss of PDL and alveolar bone

640
Q

what is the mechanism of epithelial down growth

A

growth until intact connective tissue is reached, compensation for the loss of mechanical stability

641
Q

what occurs in periodontal surgery

A

insertion of membrane which prevents cells from growing down (guided tissue regen) formation of fibrin clot against root surface

642
Q

what occurs in guided tissue regeneration

A

the insertion of membrane allows new tissue regeneration, bone can regenerate and connective tissue reformed with new fibroblasts and collagen

643
Q

what is the depth of gingival sulcus in health gingiva

A

0.5-2mm

644
Q

what is the depth of pocketing in diseased gingiva

A

> 3mm

645
Q

what is the oral mucosa

A

continuum from the gingiva and lines the whole mouth

646
Q

where are the oral epithelium and epidermis derived from

A

embryonic ectoderm

647
Q

what is the buccopharyngeal membrane

A

early structure where the epithelial from the ectoderm meet the epithelia from the endoderm

648
Q

where do oral cancers occur more commonly

A

in the pharyngeal region (inside) formed by endoderm

649
Q

what are the landmarks in the oral cavity

A

oral vestibule

oral cavity proper

650
Q

what is the oral vestibule

A

the space between the lips, cheeks, alveolar bone and gingiva. Slit-like space between lips/cheeks and alveolar bone/teeth

651
Q

what are the features of the oral vestibule

A

vestibular fornix
upper labial frenlum
frenlum near maxillary molars

652
Q

how is a midline diastema caused between the maxillary central incisors and how can this cause problems clincally

A

a large labial frenlum with an attachment site near the alveolar crest

can affect the stability of dentures

653
Q

how is the oral vestibule separated from the oral cavity proper

A

by alveolar bone/teeth

654
Q

what are the features of the oral cavity proper

A

anterior pillar of the fauces (palatoglossal fold)- formed by glossopalatine muscle
posterior pillar of the fauces (palatopharyngeal fold) - formed by pharyngopalatine
palatine tonsil
uvula
soft palate
hard palate

655
Q

what is oral mucosa made from

A

epithelium-mesenchyme

656
Q

what are the functions of the oral mucosa

A
mechanical protection-masticatory forces
barrier to microorganisms and toxins 
immunological defence (immediate and adaptive)
lubrication and buffering 
sensation
657
Q

what are the regional variations of the oral mucosa and functional adaptations

A
epithelial thickness
degree of keratinisation 
interface with connective tissue 
composition of connective tissue 
presence or absence of a submucosa
658
Q

how much of the oral mucosa consists of lining mucosa

A

60%

floor of the mouth, cheeks etc.

659
Q

how of the oral mucosa consists of masticatory mucosa

A

25%

mainly the hard palate

660
Q

how much of the oral mucosa consists of specialised mucosa

A

15%

dorsal surface of the tongue

661
Q

what is the basic architecture of oral mucosa and skin

A
oral epithelium (epidermis)
lamina propria (dermis)
submucosa (hypodermis)
662
Q

what does the oral epithelium (epidermis) consist of

A

stratified squamous epithelium

  • epithelial ridges
  • epithelial projections
  • keratinocytes
663
Q

what does the lamina propria (dermis) consist of

A

connective tissue

  • papillae
  • fibroblasts, macrophages, lymphocytes
  • collagen (I, III) and elastic fibres
  • blood vessels and nerves
664
Q

what does the submucosa (hypodermis) consist of

A

loose connective tissue: fibroblasts

  • larger blood vessels and nerves
  • fat deposits
  • salivary glands
  • found in cheeks, lips, lateral palate(no clear boundary with lamina propria)
  • much looser than the lamina propria to provide tissue mobility
665
Q

where about does the submucosa provide mobility and act as a cushion

A

in lining mucosa

666
Q

where is mucoperiosteum found

A

masticatory mucosa in the middle of the hard palate or the gingiva

667
Q

what is the regeneration cycle time for the skin and oral mucosa

A

skin- 27 days

oral mucosa- 9-14 days

668
Q

what does the stratified squamous epithelium of the oral mucosa consist of

A

basal cell layer
prickle (suprabasal) cell layer
granular layer
keratinised layer

669
Q

what are the characteristics of the basal cell layer -stratum besale

A

Cuboidal cells; proliferating

single cell layer; basal lamina attached to lamina propria;

contains stem cells and transit-amplifying cells (regeneration);

expresses keratins 5 (Type II, Basic) and 14 (Type I, Acidic)

670
Q

what can keratins be used as

A

molecular markers e.g. to diagnose cancer

671
Q

what are the characteristics of the prickle (suprabasal) cell layer - stratum spinosum

A

round, “spiny” cells (increase in desmosomes);

several layers;

differentiating;

only parabasal cells proliferate;

expresses keratins 1 and 10, loricrin and involucrin

672
Q

what are the characteristics of the granular layer- stratum granulosum

A

Larger, flatter cells; several layers

maturating

loss of cell organelles and cytoplasm filled with keratohyaline granules (contain profilaggrin and lipids; secreted)

673
Q

what are the characteristics of the keratinised layer (stratum corneum)

A
  • Very flat cells; ~20 cell layers;
  • cornified (dead); no cell organelles (nucleus)
  • filaggrin binds keratin filaments together (“keratin”);
  • crosslinking of involucrin→ cornified envelope (barrier);
  • cell shedding (desquamation)

Cornified envelope forms a barrier against microorganisms

674
Q

what are the types of keratinisation and where are they found

A

orthokeratinised- hard palate, tongue
parakeratinised- gingiva
nonkeratinised- lining mucosa

675
Q

what is orthokeratinised

A

cornified layer: dead cells, no cell nuclei

676
Q

what is parakeratinised

A

cornified layer: dead cells,

cell nuclei present

677
Q

what is nonkeratinised

A

superficial layer: live cells

no keratohyalin granules

678
Q

what are they other cell types (“clear cells”) in oral mucosa

A

melanocytes- basal; produce melanin pigment and transfer it to keratinocytes via dendritic processes

Merkel cells: Basal; sensory receptor cells => sense light touch

Langerhans cells (immune cells) : Suprabasal; dendritic cells; antigen processing & presenting to immune system

Lymphocytes: Often associated with Langerhans cells; Inflammatory response

679
Q

what is the mucosa for the hard palate

A

masticatory mucosa

680
Q

what are the features of the hard palate

A

Incisive papilla: Prominence overlying nasopalatine foramen (→ denture fitting).

Palatine raphe: Midline epithelial ridge; directly attached to bone

Palatine rugae: Unique epithelial folds; food transport towards pharynx

Alveolar bone: Submucosa present at junction with lateral hard palate

Fovea palatini (openings of the ducts of minor salivary glands; posterior border for an upper denture)

681
Q

what are the landmarks in the hard palate important for denture fitting

A

incisive papilla

fovea palitini

682
Q

what are the histological features of the masticatory mucosa

A

thick epithelium
can be OC or OC+PK

lamina propria

  • long, narrow papillae
  • dense collagen fibres

mucoperiosteum (submucosa) absent

683
Q

what type of mucosa is buccal mucosa

A

lining mucosa

684
Q

what are the features of buccal mucosa

A

fordyce’s spots
parotid papilla- level of 2nd max molar, opening of parotid duct
linea alba- parakeratinisation of buccal mucosa at moar occlusal plane

685
Q

what are fordyce’s spots and what is their production and function

A

Ectopic sebaceous gland without associated hair follicle

Sebum (oily substance) lubricates the buccal mucosa or the lips

686
Q

what is present on the skin of lip epithelium

A

keratinised epidermis
hair follicle
sebaceous gland
dermis

687
Q

what mucosa is on the floor of the mouth

A

lining mucosa

688
Q

what are the features on the floor of the mouth

A

Lingual frenum
Sublingual papilla- opening of the submandibular salivary ducts
Sublingual folds- openings of the sublingual salivary ducts
Fimbriated folds- irregular folds; remnants of tongue development
Deep lingual veins

689
Q

outline the histology of lining mucosa: labial and buccal

A
Epithelium:
-Thick; Nonkeratinised
Lamina Propria:
-Dense; Long and slender papillae
Submucosa:
-Dense; firmly attached to muscle;  minor salivary and sebaceous glands
-Function: Mobility and Stability
690
Q

outline the histology of lining mucosa: ventral tongue;floor of mouth

A
Epithelium:
-Thin; Nonkeratinised
Lamina Propria:
-Thin; Short papillae
Submucosa:
-Thin and irregular
-Function: Mobility
691
Q

outline the features of the lips(lining mucosa) and gingiva (masticatory mucosa)

A
  • Vermillion zone: Lining mucosa
  • Intermediate zone; parakeratinised
  • Labial mucosa: Lining mucosa; nonkeratinised
  • Alveolar mucosa: Lining mucosa; nonkeratinised
  • Gingiva: Masticatory mucosa; parakeratinised (+ orthokeratinised)
  • Mucogingival junction: Junction between alveolar mucosa and gingiva
692
Q

what is the vermillion zone of lining mucosa and what are its characteristics

A

Transition zone between skin and labial mucosa

Keratinised. Thin epithelium; numerous capillaries => red colour; contains no salivary glands, only a few sebaceous glands in corner of the mouth.

693
Q

what are the functions of the tongue

A

Mastication, swallowing, speech, taste, immune function

694
Q

what are the ectodermal appendices on the tongue

A

filiform papillae- masticatory
fungiform papillae-taste
foliate papillae- taste circumvallate papillae - taste

695
Q

where is the epithelium derived from on the anterior 2/3 of tongue

A

ecotoderm

696
Q

where is the epithelium derived from on the posterior 1/3 of tongue

A

endoderm

697
Q

what is the histology of the specialised mucosa: dorsal surface of the tongue and what is its function

A

Epithelium:
- Thick
- Orthokeratinised (filiform papillae)
Nonkeratinised (taste papillae and interpapillary regions)

Lamina Propria:

  • Long papillae
  • Nerves, minor salivary glands

Submucosa:
-Absent (lamina propria attaches directly to muscle)

Function: Stability & Taste

698
Q

what are the age changes of the oral mucosa

A

Smoother and dryer surface (→ ‘dry mouth’)

Thinner epithelium, flattening of epithelial ridges (arrow)

Decreased cellularity of lamina propria and increase in fibrous tissue (asterisk; fibrosis)

Fewer Langerhans cells (reduced immunity)

  • Systemic disease
  • Medication (decreasing salivary flow)

Increase in Fordyce’s spots (buccal, lips)

Atrophy of minor salivary glands

699
Q

what are the age related changes of the tongue

A

Epithelial atrophy (loss of FF papillae)

  • smooth, often fissured surface
    (e. g. nutritional deficiencies; medication)

Burning sensations; loss of taste – poorly understood

Development of nodular, varicose veins on underside of tongue (‘caviar tongue’)

700
Q

what is black hair tongue

A

Hypertrophy of filiform papillae - TOO MUCH FILLIFORM PAPILLAE

The papillae trap food, accumulation of food debris and microorganisms

701
Q

what is geographic tongue

A

(Benign migratory glossitis)

Atrophy (loss) of filiform papillae; migrating depapillated patches with white border; inflammation (arrows)

occurs in children

702
Q

what is recurrent aphtous stomatitis

A

Painful lesions in the mouth
Recurrent mouth ulcers
20% of population (familial history)
starts in childhood or adolescence

703
Q

what are other types of ulcers

A
Virus infections (e.g. Herpes, HIV)
Iron and vitamin B deficiency
Crohn’s disease
704
Q

what is candida albicans infection

A
  • Fungal hyphae (stained purple)
  • Older ages
  • Shows up at white spots
  • Fungal hyphae in the stain
705
Q

what are the common diseases of the oral mucosa

A

recurrent aphtous stomatitis

lichen planus- reticular patches (autoimmune disease)

white sponge naevus- spongy

leukoplakia- white patches

706
Q

what are the solutions to the problems of tissue regeneration e.g. there is incomplete tissue function regeneration

A

cellular therapy- stimulate bodys own stem cells into repairing defect
tissue engineering - collagen netword to modulate tooth shape
biomedical engineering
gene therapy- altering genome

707
Q

what are stem cells and what is their function

A

Unspecialised (undifferentiated) cells that:

  • can self-renew
  • can differentiate into other cell types

Function: Development and Regeneration (become active in an injured tissue)

708
Q

what are totipotent stem cells

A

all cell types (e.g. fertilised egg)

709
Q

what are pluripotent stem cells and where are they found

A

all cell types of the three embryonic germ layers (e.g. embryonic stem cells)

rare, not accessible in the adult body.

710
Q

what are multipotent stem cells

A

many cell types (e.g. haematopoietic stem cells; mesenchymal stem cells)

711
Q

what are oligopotent stem cells

A

few cell types (e.g. Myeloid precursors -Five blood cell types)

712
Q

what are quadripotent stem cells

A

four cell types

(e.g. mesenchymal progenitor cells: cartilage, bone, stroma, fat)

Unipotent: one cell type (e.g mast cell precursors)

713
Q

what are the 4 tissues of tissue regeneration

A
  1. Stem cell-mediated regeneration
  2. Epimorphosis
  3. Morphallaxis
  4. Compensatory regulation
714
Q

what is involved in stem cell mediated regeneration and what are examples

A

Replacement of lost tissue by stem cell activity. Production of new progenitors

Examples: Hair growth from follicular stem cells in the hair bulge.

715
Q

what is involved in epimorphosis and what are examples

A

Dedifferentiation of cells at the wound site and formation of undifferentiated cells that redifferentiate to form the lost structure.

Example: Planarian flatworms; Amphibian limbs

716
Q

what is involved in morphallaxis and what are examples

A

Repatterning of existing tissue with little new growth.

Example: Hydra (freshwater polyp- if you cut across middle)

717
Q

what is involved in Compensatory regulation

A

Differentiated cells divide and maintain their differentiated functions

Example: Liver regeneration- liver injury, the cells start to divide again and maintain their function

718
Q

what are the 4 stages of wound healing in the oral mucosa

A

Hemostasis
Inflammatory response
Reparative phase (epithelial response)
Reparative phase (connective tissue response)

719
Q

what occurs in stage 1- Hemostasis

A
  • Vascular damage causes hemorrhaging into the tissue defect and results in the formation of a blood clot (Coagulation: fibrin deposition & aggregation of platelets)
  • Forms barrier that unites the wound margins and protects the exposed tissue; provides provisional scaffold for subsequent colonisation by reparative cells.
720
Q

what occurs in stage 2- inflammatory response

A

Cell activation, migration and function

Microorganisms and toxins have likely entered through the wound and induce an acute inflammatory response

Leakage of plasma proteins and platelet-derived cytokines and growth factors

leukocyte migration towards the wound

Neutrophils- kill bacteria (appear within a few hours)
Monocytes- remodelling
lymphocytes- humoral
(appear after 24hrs)

721
Q

what occurs in stage 3: reparative phase

A

epithelial response

Mobilisation of epithelial cells
within 24 hours

Increased basal cell proliferation and epithelial cells adjacent to the wound margin start to migrate beneath the blood clot (24-48 hours). basal lamina deposition facilitates movement and epithelial sheet formation (stratification- squamous stratified ep produced)

Migration stops when cells reach opposing wound margin and increased cell proliferation and differentiation leads to stratification

722
Q

what occurs in stage 4: reparative phase

A

connective tissue response
Fibroblasts proliferate and migrate into wounded connective tissue within 24- 48 hours and deposit disorganised collagen fibres

Formation of new blood capillaries from existing vessels (angiogenesis) at the wound margin ECM (fibronectin, laminin, collagen) formed by new fibroblasts provides scaffold for forming blood vessels.

scar tissue formation-Increased collagen deposition between days 5 and 20 but reduced tensile strength

723
Q

what is fibroblast deposition of collagen regulated by

A

TGF-β

724
Q

what is the Formation of new blood capillaries from existing vessels (angiogenesis) at the wound margin regulated by

A

VEGF, FGF and TGF-β

725
Q

what does the formation of new capillaries provide

A

nutrients and oxygen, enable access of inflammatory cells, stimulate connective tissue formation

726
Q

what happens to the scar tissue

A

its remodelled and converted into better alignment of collagen fibres in around 5 months

727
Q

outline what occurs in wound contraction

A

First fibroblasts to enter the wound site are contractile myofibroblasts and Pull the wound together

Different from connective tissue fibroblasts

Pericytes implemented in the formation of myofibrocytes- pull wound together

Form connections with each other and with collagen fibrils → alignment

Contraction draws edges of the wound together

728
Q

what are the features of scar tissue

A

inferior quality
deposition of disorganised collagen leads to immobilisation and rigidity at repair site
remodelled in oral mucosa - wound regenerates to normal function

729
Q

why do injuries during development result in scarless healing

A

they do not involve the inflammatory response

730
Q

how does wound healing occur following tooth extraction

A

repair:
tooth socket fills with a clot

epithelial response:
epithelialisation of socket (by day 10)

inflammatory response:
polymorph and macrophage response
osteogenic precursors migrate into blood clot

proliferation phase:
osteoblasts differentiate and form bone

731
Q

how does wound healing occur at the dento-gingival junction

A

Day 3: Colonisation of gingival wound by epithelial cells and formation (regeneration) of the junctional epithelium

Day 5-7: Expansion and down-growth of the junctional epithelium. Re-establishment of dento-gingival junction

732
Q

what is the difference in the restoration of a fucntional unit to the oral mucosa

A

PDL fibres must insert into cementum and bone

Coordinated repair requires complex regulation at cellular and molecular level

733
Q

what are the cell types involved in the repair of periodontal tissue and what is their function

A

Fibroblasts- remodelling collagen fibres

Endothelial cells- form new blood vessels from existing vessels

Cementoblasts- perivascular and endosteal fibroblasts

Osteoblasts- mesenchymal progenitor cells in the endosteum or periosteum

734
Q

what occurs in the normal process of periodontal tissue repair

A

No inflammation, e.g. tooth movements

735
Q

what occurs in injury process of periodontal tissue repair

A

Inflammatory response required to combat infection and initiate repair

736
Q

why can endogenous repair not be restored if the tissue is chronically inflamed

A

chronic inflammation inhibits stem cell activation, cell recruitment, cell proliferation and differentiation so cannot restore tissue function

737
Q

what occurs in mild periodontal inflammation

A

Dental plaque accumulation causes inflammatory response in connective tissue.
-70% of collagen fibres destroyed within 3-4 days!

738
Q

what does persistent inflammation cause in PD

A

Further destruction of connective tissue by inflammatory cells
causes apical migration of junctional epithelium (arrow)
Formation of gingival pocket.
Advanced: Loss of PDL and alveolar bone.

739
Q

how far does epithelial down growth go

A

Growth until intact connective tissue is reached

Compensation for loss of mechanical stability.

740
Q

whats involved in periodontal surgery

A

Insertion of membrane (physical barrier).
Guided tissue regeneration
preventing abnormal wound healing by inducing the clot

741
Q

what are the molecular approaches in periodontal repair in PDL and cementum

A

EGF, FGF, IGF, PDGF, TGF-ß

742
Q

what are the molecular approaches in periodontal repair in bone and cementum

A

BMP

743
Q

what does fibronectin do

A

Forms a link between the fibroblasts and collagen fibres

744
Q

what does enamel matrix (emdogain) do

A

Cementum formation may stimulate periodontal repair. Loss of bone in PD- reinduction if new bone in the area required to save the tooth

745
Q

what is the physio-chemical repair process of enamel

A

Remineralisation by calcium, phosphate and fluoride ions in saliva

746
Q

what is the dynamic process of early caries lesions

A

can be reversed

WSL reversible if surface enamel intact (underlying body may contain destroyed enamel prisms) and acid producing bacteria are removed

remineralisation by ion precipitation from saliva

747
Q

what does the dentine reparative process depend on

A

Extent and duration of stimulus
Structural variations in dentine:open or occluded dentinal tubules
Age of tooth:Smaller pulp chamber, diminished blood and nerve supply

748
Q

how does dentine reparative process occur after slow onset due to prolonged insult (attrition, early caries )

A

Occlusion of dentinal tubules: Collagen plug or sclerotic dentine – closes up tubules

Reactionary dentine in the pulp: formed by existing odontoblasts (slow, tubular)

749
Q

how does dentine reparative process occur rapid onset due to severe insult (late stage caries, cavity prep)

A

Reactionary dentine: could form if odontoblasts survive (slow, tubular)

Reparative dentine: formed by newly differentiated odontoblast-like cells if original odontoblasts have died (rapid, amorphous, less collagen

750
Q

what are the dental stem cell sources for dental regeneration

A

e. g. from 3rd molars; primary teeth:
- Dental pulp (DPSC)
- Dental pulp from exfoliated primary teeth (SHED)
- Dental follicle of unerupted teeth
- Periodontal ligament (PDLSC)
- Root apical papilla (SCAP) Tooth germs
- Epithelial rests of Malassez

751
Q

what are the opportunities in dental tissue engineering and regeneration

A
  1. Tissue engineering:
    a) Biodegradable scaffolds for cell seeding; 3D printing
    b) Bioengineering, material sciences and nanotechnology:
    - Nano)materials with novel properties that can be stimulate biological tissues
    c) Implants with bioactive surfaces allowing for better tissue integration.
  2. Gene therapy: Ex vivo or in vivo
    • CRISPR/Cas9 genome editing tools; RNAi; novel viral delivery vectors
    • May not be applied well in dental practice
752
Q

what is the potential impact of tissue engineering and regeneration on future clinical practice, what are the limitations

A

Conventional: amalgam, composites, metallic implants, tissue grafts.

Limitations: non-biological, immune rejection, pathogen transmission, lack of remodelling with recipient tissue, donor site morbidity.

Novel: Engineering of precise tissue shape using biodegradable scaffolds onto which cells can grow and re-establish morphology and function.

753
Q

when force is applied to the crown, where is the force transmitted to

A

to the root and then to the cementum in the PDL and to the bone.

754
Q

what is the anatomy of the PDL

A

Collagen
Vascular supply
Nerve endings – pain & proporioception
Fluid – shock absorber
contains undifferentiated mesenchymal cells → fibroblasts & osteoblasts

755
Q

what is the anatomy if bone

A

osteoblasts
osteoclasts
osteocytes

756
Q

when force is applied to the crown, where is the force transmitted to

A

to the root and then to the cementum in the PDL and to the bone.

757
Q

what is the anatomy of the PDL

A

Collagen
Vascular supply
Nerve endings – pain & proporioception
Fluid – shock absorber
contains undifferentiated mesenchymal cells → fibroblasts & osteoblasts

758
Q

what is the anatomy of bone

A

osteoblasts
osteoclasts
osteocytes

759
Q

what is the response of the PDL and bone to normal function e.g. a force of very short duration

A

PDL doesn’t compress, alveolar bone bends which sends a piezoelectric signal

760
Q

what is the piezoelectric function

A

force applied to crystalline structure (bone/collagen)

movement of electrons

short flow of current

761
Q

what is the response to forces of 1-2 seconds

A

PDL fluid expressed

Tooth moves in socket

762
Q

what is the response to forces of 3-5 seconds

A

PDL fluid redistributed

Tissue compressed- pain

763
Q

what is the response to forces of longer duration

A

tooth moves in socket

bone changes occur

764
Q

what are the electrical signals and pressure tensions that occur in response to orthodontic forces

A

Piezoelectric effect

Streaming potential- movement of ground substance

Change in blood flow- increase in tension, decrease in compression

Microfractures- hyalinisation

  • Chemical signals- e.g. prosdaglandins, IL-1, Leukotrienes, MMPs
  • Cellular response- osteoblasts, osteoclasts, osteocytes
  • Systemic response- PTH, VitD, Calcitonin etc.
765
Q

what is the effect at duration and level of force

A

force tooth

PDL and bone biological electricity & pressure-tension

osteoblasts (tension) and osteoclasts (compression)

bone resporption/deposition

766
Q

What happens when heavy ‘orthodontic’ forces are applied after 3-5s

A

blood vessels in PDL occluded on pressure side

767
Q

What happens when heavy ‘orthodontic’ forces are applied after a few Mins

A

blood flow cut off to compressed PDL area

768
Q

What happens when heavy ‘orthodontic’ forces are applied after a few Hours

A

Cell death in compressed area- hyaline layer. Bone adjacent to squashed PDL doesn’t have a blood supply

769
Q

What happens when heavy ‘orthodontic’ forces are applied after 3.5 days

A

Cell differentiation, undermining resorption starts

770
Q

What happens when heavy ‘orthodontic’ forces are applied after 7-14 days

A

undermining resorption removes lamina dura, tooth movements

771
Q

What happens when light ‘orthodontic’ forces are applied after 3-5s

A

blood vessels in PDL

  • Pressure side- partially compressed on pressure side
  • Tension side- dilated
772
Q

What happens when light ‘orthodontic’ forces are applied after a few mins

A

blood flow altered, this allows release of cytokines

773
Q

What happens when light ‘orthodontic’ forces are applied after a few hours

A

metabolic changes

  • Chemical messengers- cellular activity
  • Enzymes
774
Q

What happens when light ‘orthodontic’ forces are applied after 4 hrs

A

cell differentiation in PDL e.g. osteoclasts and osteoblasts

775
Q

What happens when light ‘orthodontic’ forces are applied after 2 days

A

tooth movement more gradual by remodelling

776
Q

outline the ways in which teeth can move

A
Tipping 
Translation/ Bodily Movement
Rotation
Extrusion
Intrusion
777
Q

what occurs in tipping

A

Simple movement

Around centre of resistance

Tips the tooth 1/3 from apex

Forces greatest furthest from CoR- forces on the tooth are greatest at the apex.

Can be achieved by any appliance

Force 50-75g

778
Q

what occurs in translation

A

Harder to achieve- moving tooth through the bone

All PDL uniformly loaded

Force 100-150g

779
Q

what occurs in Rotation

A

Theoretically need high force BUT

Tipping occurs → Excessive compression of PDL

Force – 50-100g

Not too hard to achieve with fixed appliance

780
Q

what occurs in Extrusion

A

Pull out the bone

Produce tension in PDL fibres- don’t want too high of a force or risk of loss of vitality of tooth

Force 50-100g

781
Q

what occurs in Intrusion

A

Push into the bone

Forces concentrated at root apex

Fairly low force Force 15-25g

Missing part of tooth- tooth moved with too heavy of force, damage to cementum, osteoclasts get to the dentine and caused root resorption

782
Q

what are the Risks Orthodontics to the pulp

A

Transient inflammatory response

Can cause loss of vitality

783
Q

what are the Risks Orthodontics to the root

A

Root resorption inevitable

Commonly decreased 1-2mm root length

Some repair – however only ever filled in by cementum (rest periods)

Increased with: Distorted apices (roots bend) , Thin roots, Compromised teeth, Excess force, History of root resorption, Asthma

784
Q

what are the Risks Orthodontics to the bone

A

Minimal transient damage

BUT : lose ½-1mm of alveolar crest

785
Q

what are the Risks Orthodontics to the PDL

A

Minimal transient damage

Unless: Excess force maintained, Existing periodontal disease, Important in relapse- teeth go back to where they were

786
Q

what are the Risks Orthodontics to the Cementum

A

Protects tooth from root resorption

Limited capacity to repair

787
Q

what occurs in Ankylosis and why

A

Tooth won’t move

In growing patient causes infraocclusion

Root fused to the bone

Periodontal ligament lost, bony union between tooth and bone

Tooth sounds ‘tinny’ on percussion.

Aetiology often trauma

788
Q

why is consent for orthodontic treatment important

A
  • Root resorption
  • Ankylosis
  • Decalcification
  • Retention / relapse
789
Q

what occurs in Overeruption of teeth and what are the problems associated with this

A

teeth tend to continue to erupt if no occlusal contacts- Tendency for teeth to erupt to maintain contact

Problems: gingival trauma , restoration difficult, occlusal problems

Not inevitable- within limits bone/growth

Importance: restorations

Anterior wear- continue to erupt and maintain contact

790
Q

what occurs in mesial drift and why might this occur

A

Teeth drift mesially

Maxilla > mandible

Early loss of primary teeth- space loss so posterior teeth drift

Importance to space maintain

Mesial drift can be useful- if early loss of first molars, second molars can erupt mesially

791
Q

why might Late lower incisor crowding occur

A

Mandible continue to grow after maxilla stops, mandibular teeth don’t have anywhere to go so stay crooked.

other theories
pressure from Third molars? Mesial drift?

792
Q

what occurs in the discolouration of teeth due to age changes

A

progressive thinning of enamel due to tooth wear and thickening of dentine produces yellowish teeth

stains become trapped in microscopic pits of enamel during enamel remineralisation

793
Q

what might tooth staining result in (in terms of enamel development)

A

pronounced striae of retzius

794
Q

how do whitening agents work

A

produce free oxygen radicals that penetrate through the enamel pores and reduce large chromogenic molecules to smaller molecules that might diffuse out of the pores or absorb less light.

795
Q

why are older people less susceptible to caries

A

over time the enamel surface becomes more mineralised by incorporation of fluoride present in saliva- this forms fluorapatite rather than hydroxyapatite, which is more resistant

796
Q

what is involved in the physio-chemical repair process of enamel

A

Remineralisation of enamel by re-incorporation of calcium, phosphate and fluoride ions that are present in saliva

797
Q

what occurs when there is an imbalance in the de-/re- mineralisation cycle

A

Shift towards demineralisation causes caries. Earliest sign on teeth: ‘White spot lesion’

798
Q

what is the difference clinically between a chalk-white lesion and hypomineralised lesion of developmental origin

A

hypomineralised lesions have a shiny appearance, whereas chalk-white lesions don’t (they’re active and non cavitated)

799
Q

what does the dark zone and translucent zone represent

A

Dark zone: enamel remineralisation is ongoing

Translucent zone: enamel demineralisation

800
Q
how do the enamel colours for:
surface zone
body of lesion 
dark zone
translucent zone 

differ in transmitted light and polarised light

A

transmitted v polarised

Surface zone:
Greenish/brown → Blue

Body of lesion: Orange → ‘Light’ black

Dark zone: Black → ‘Dark’ black

Translucent zone: Not visible here

801
Q

what might the dark colour of enamel in ground sections represent

A

may represent a combination of enamel staining and hypomineralised enamel undergoing remineralisation, or where a WSL has developed, but has been arrested over time.

802
Q

where does secondary dentine accumulate and what does this lead to

A

lines the pulp and root canals after the completion of tooth roots
more common on the roof and floor of pulp chamber (masticatory forces directly act in the cusp region)

pulp recession

803
Q

what are the histological features of secondary dentine

A

continuous with primary dentinal tubules but fewer in number due do odontoblast death

contour line of owen- tubules can bend between primary and secondary dentine

804
Q

where does peritubular dentine form

A

on the walls of dentinal tubules

Begins to form in outermost dentine

805
Q

what are the characteristics of peritubular dentine

A

About 90 % mineralised
Usually does not contain collagen
Can fill whole dentinal tubules

806
Q

what occurs when peritubular dentine completely occludes dentinal tubules

A

formation of sclerotic dentine

807
Q

outline the physiological and pathological formation of sclerotic dentine

A

Physiological:

  • Ageing process
  • Found mostly in roots

Pathological:

  • Response to caries
  • It is Found between carious lesion and pulp- in the dentine directly affected by progression of caries lesion
808
Q

when is tertiary dentine produced

A

Reactionary dentine: slow response mediated by existing odontoblasts lining the dental pulp, fewer tubules. => response to tooth wear (attrition)

Reparative dentine: rapid response mediated by new odontoblast-like cells induced from dental pulp stem cells (existing odontoblasts have died), less structure. => response to caries or cavity preparation

809
Q

what can stimulate peritubular dentine formation

A

slow, natural wear of the crown

810
Q

what is the response by dentine to tooth wear(attrition)

A

peritubular dentine formation

dentine becomes less permeable and insensitive if exposed

reactionary dentine forms in the pulp to compensate for dental tissue loss

811
Q

what are the differences between old and young teeth due to reactionary dentine

A
Young tooth:
•	Little tooth wear
•	Larger pulp volume
•	Defined pulp horn
•	Pulp volume large
Old tooth:
•	Worn cusp
•	Smaller pulp  volume
•	Pulp horn filled in with reactionary dentine to compensate for tissue loss
•	Narrowed root canal – due to ageing as well
812
Q

how do dead tracts form

A

Group of odontoblasts die due to continuous, strong stimulus

Results in reparative dentine formation that acts to seal off the pulp from invading micro- organisms

The tubules do not contain odontoblast processes anymore

Empty dentinal tubules contain air causing a dark appearance on ground sections

813
Q

what are the age changes in the dental pulp

A

Decreased number of cells (e.g. odontoblasts)

size reduction of the pulp chamber

Calcified structures in pulp

814
Q

what is the difference between the calcified structures in the pulp:

  • false pulp stones
  • true pulp stones
  • diffuse calcifications
A

False pulp stones: Have not been produced by odontoblasts, they are calcified areas characterised by Concentric layers of calcified degenerated pulp tissue.

True pulp stones (Denticles):

  • Produced by true odontoblasts
  • Organic matrix and dentinal tubules

Diffuse calcifications:

  • Through the pulp
  • Usually associated with blood vessels or collagen fibres- as you age blood vessels can calcify
815
Q

what are the ages changes that occur in cementum

A

Cementum thickness increases 3x from 16-70 years of age

Cellular cementum- Forms at root apex in response to attrition at the occlusal surface

816
Q

what is hypercementosis and how does it occur

A

increase in cementum

  • response to physiological process such as attrition
  • Pathological process causing excessive build up
817
Q

what are the age changes in the PDL

A

Decrease in cell numbers, density and mitotic activity

Fibroblasts have shorter live spans and diminished collagen synthesis and degradative activity

Increased collagen fibrosis, thicker fibre bundles and mineralisation of fibres

Irregular insertions of Sharpey’s fibres

Teeth become less “mobile” (→ decreased remodelling capacity able to move teeth in the jaw)

818
Q

what are the Age changes that occur in alveolar bone

A

Loss of teeth => loss of alveolar bone

819
Q

what are the Age changes in oral mucosa

A

Thinning of tongue epithelium on dorsal and lateral surfaces (oral cancer)

Reduced taste sensation

Gingival recession – but may be unclear if due to decreased oral hygiene or normal age change

Increasing susceptibility to precancerous lesions and oral cancer

820
Q

what are the Age changes in salivary glands

A

Decrease in amount of glandular tissue

Increase in fibrous tissue, fat cells and inflammatory cells.

Dry Mouth (Xerostomia):

  • Usually not presented in healthy older people
  • Associated with increased use of medications
  • Increases the rate of attrition (due to reduced enamel mineralisation
821
Q

what is Physiological attrition and what does it affect. what type of dentine forms in response

A

natural process - tooth wear caused by mastication, e.g. contact with food particles

Affects interproximal and occlusal surfaces

Reactionary dentine has formed in response to attrition and blocked off the dentine tubules, which have become dead tracts.

822
Q

what is pathological attrition

A

tooth wear caused by chewing with abnormal movement or habitual jaw clenching, e.g. bruxism

823
Q

what is abrasion

A

tooth wear caused by frictional contact with foreign objects, e.g. pipe smoking

824
Q

what is erosion and what are the dietary, environmental and medical causes

A

progressive loss of hard tissues due to chemical dissolution

Dietary: e.g. carbonated drinks, fruit/citrus juices and other acidic drinks and foods.

Environmental: e.g. competitive swimmers & professional wine tasters

Medication: e.g. Iron tonics, vitamin C and nutritional supplements.

825
Q

what is bruxism

A

Pathological attrition
Habitual jaw clenching and tooth grinding:

Flat occlusal plane

Dentine hypersensitivity due to exposed dentine

826
Q

what occurs in tooth brush abrasion

A

V-shaped cervical lesions due to:
• excessive tooth brushing
• abrasive toothpastes

827
Q

how is erosion caused by stomach acid

A

Regurgitated stomach acid
• Acid reflux or repeated vomiting
• Eating disorders: Anorexia, Bulimia
• After vomiting, tooth brushing should be avoided for one hour

828
Q

what is the Chemical basis for erosion

A

Enamel doesn’t dissolve in calcium-phosphate super-saturated saliva (pH 7) but at pH < 6, saliva is under-saturated and cannot efficiently remineralise the acid.

Acidic dissolution initiates erosion and makes the tooth more susceptible to abrasion.

The lower the pH of the oral environment, the higher is the enamel surface loss.

829
Q

what Factors contribute to dietary erosion

A

Amount of drink consumed

Frequency & manner of consumption

Timing of consumption

Strength of acid

830
Q

what are Lesser known risk groups

A
  • Diabetics who consume fruit juice
  • People who have low salivary flow (e.g. older people on medication) should avoid acidic drinks
  • Children with asthma (Inhaling lowers the pH)
  • Consumers of sports drinks (high sugar)
  • Ecstasy and cocaine users
831
Q

what are the 4 parameters that caries needs to occur

A

host
diet
time
microbes

832
Q

what are the clinical aspect of the development of caries

A

subsurface translucent zone
development of dark zone
early WSL
cavitation, spread along ADJ, relative changes in dentine

833
Q

what is the ‘seal’ and ‘hold’ concept

A

can arrest the decay if just filled with a sealant

834
Q

what is the hall technique

A

caries is arrested as a metal crown is placed over the tooth, which will remove the substrate going to the caries

835
Q

outline what is involved in the overview of pain diagnosis

A
dentine hypersensitivity 
reversible pulpitis
irreversible pulpitis 
apical periodontitis (asymptomatic/symptomatic)
peri-apical abscess (acute/chronic)
836
Q

what is dentine hypersensitivity

A

short sharp pain arising from exposed dentine in response to stimuli (e.g. periodontitis so dentine exposed due to gum recession)

837
Q

what are the stimuli for dentine hypersensitivity

A

thermal, evaporative, tactile, osmotic (e.g. draws fluid through tubules) or chemical

838
Q

what is hydrodynamic theory

A

rapid shifts of fluid within the dentinal tubules, following stimulus application, results in activation of sensory nerves in the inner dentine region of the tooth

839
Q

what are the 3 theories of dentine hypersensitivity

A
  1. dentine innervated directly
  2. odontoblasts act as receptors
  3. odontoblasts at the base of odontoblasts are stimulated directly or indirectly by fluid movement through the tubules
840
Q

how can sensitivity be managed

A

block tubules
de-sensitising agents
adhesive restorations- physically block tubules
elective devitalisation- remove the nerve from the tooth

841
Q

how can sensitivity occur due to bleaching (hydrogen peroxide)

A
  1. removal of dentinal tubule plugs by oxygenating bleaching gels that remove micro debris within the tooth
  2. outward movement of fluid within the dentinal tubules due to osmosis from bleaching gels
842
Q

what occurs in cracked cusp syndrome

A

Tooth with crack or fracture

Exhibits a sudden sharp pain- fluid pushed through the tubules

Usually on mastication and classically on release of pressure.

Non vital teeth/ obturated teeth can give ‘dull ache’ and be sensitive to mastication.

843
Q

how can cracked cusp syndrome be diagnosed

A

History

Orthodontic band

Transillumination- shine light through the tooth

Dyes

Magnification

Tooth sloth- specific occlusal force can be place on one cusp

844
Q

how can Cracked cusp syndrome be managed

A

Bonded restoration

‘Cuspal coverage’ (crown)

Endodontic treatment

Extraction

845
Q

what are the causes of pulpal inflammation

A

caries
defective restorations
trauma
dens investigation

846
Q

what is pulpitis

A

chronically inflamed pulp- can be painless

acutely inflamed pulp can be painful with stimuli from hot, cold, sweet

847
Q

what are the symptoms of reversible pulpitis

A

pain is short in duration
pain disappears when stimulus is removed
poorly localised

848
Q

how can reversible pulpitis be managed

A

remove irritant and restore
preserve pulp
review

849
Q

what the symptoms of irreversible pulpitis

A

Pain is longer in duration.

Pain persists (minutes to hours) when stimulus removed.

Cold can reduce pain- dental emergency clinic

Poorly localised

May have percussion sensitivity- sore when pressure applied

Spontaneous pain

850
Q

how can irreversible pulpitis be managed

A

Pulpotomy- half of pulp removed

Pulpectomy- all of pulp removed

Extraction

Not antibiotics- not bacterial infection

851
Q

what should be done in a stepwise excavation in reversible pulpitis

A

remove the worst, seal and then re-enter

852
Q

what are the types of apical periodontitis

A

Symptomatic apical periodontitis

Asymptomatic (chronic) apical periodontitis

Acute apical abscess

Chronic apical abscess

Cyst formation (radicular)- unsure why.

853
Q

what is the diagnosis for symptomatic apical periodontitis

A

TTP, can respond to sensibility tests, can have apical widening of periodontal ligament.

854
Q

what is the diagnosis for Asymptomatic (chronic) apical periodontitis

A

Not TTP, no response to sensibility tests, usually shows apical radiolucency.

855
Q

what is the diagnosis for Acute apical abscess

A

TTP, non- responsive, swelling (intra or extra-oral), febrile, lymphadenopathy.

856
Q

what is the diagnosis for Chronic apical abscess

A

As for asymptomatic apical periodontitis but with draining sinus. Can be mildly TTP.

857
Q

what would be the diagnosis for a toothache for a 10 year old patient, Fit + Well where:

  • Nature: sharp pain on stimuli, with lingering aching pain
  • Duration: 60 minutes after triggered
  • Started: 5 days ago
  • Stimuli: hot, pressure, spontaneous. (Cold helps)

and on clinical examination:

  • DO caries 55
  • Mildly TTP.
  • Marginal ridge broken down
A

Irreversible pulpitis

858
Q

what would be the provisional diagnosis for
• 10 year old patient, F+W
• Patient has ‘toothache’

Patient history
•	Nature: Constant dull aching pain
•	Duration: hours
•	Started: 7 days ago
•	Stimuli: pressure, biting.

Clinical examination
• Grossly carious 54.
• TTP

A

Acute apical periodontitis

Beyond pulpitis- pulp necrotic

859
Q

what would be the provisional diagnosis for

  • 60 year old patient, F+W
  • Asymptomatic but has ‘noticed he has a hole in his tooth’.
Patient history
•	Nature: No pain.
•	Duration: No pain.
•	Started: No pain.
•	Stimuli: No pain.
•	Just suddenly had a hole in a tooth.

Clinical examination
• 15 buccal abrasion wear cavity.
• 16 buccal abrasion wear cavity.
• Striations

A

Abrasion, abrasive tooth wear