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BDS 2 > Growth, Development and Aging > Flashcards

Growth, Development and Aging Flashcards

1
Q

when is BMI important for paediatric dentistry

A

high BMI increases risk of problems under GA

low BMI may show malnutrition

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2
Q

when are childrens rapid growths?

A

0-2 child growth
12-18 through puberty
steady growth in the middle

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3
Q

when would we make a paediatric referal in terms of BMI/height

A

if in the <3 centile or >97 centile

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4
Q

what does a baby 0-2yr old’s growth depend on

A

growth disorders / health
mothers health
nutrition
Placental efficiency

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5
Q

what is the leading cause of growth suppression

A

chronic illness e.g. undiagnosed coeliac/malnutrition

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6
Q

why is there discontinuity with heights between 1 and 3

A

change from measuring laid down to measuring stood up

spine compresses under weight so appear shorter ~2 yrold

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7
Q

what is a classic cause of short back long legs and why

A

reduced sex hormone testosterone/oestrogen

these hormones are important for back growth

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8
Q

how do we estimate the height of a child

A

take a mid parental height = should be +-10 within this

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9
Q

how do you find a mid-parental height for a boy and girl

A

((mothers height + 13) + fathers height ) / 2 = boy

((fathers height - 13) + mothers height) / 2 = girl

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10
Q

what are the limitations of current height graphs

A

don’t take into account all ethnicities

not realistic e.g. we can’t keep increasing in size by 1cm per decade forever

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11
Q

what should be taken on a weight history

A 
weight and height of siblings
weight and height of parents
birth height and weight
any illnesses of baby, siblings and parents
pregnancy details
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12
Q

when measuring height, what must we ensure

A 
take all height altering clothes off e.g. shoes
hands by side loosely
feet forward with heals against the wall
breathe in....
breathe out and measure
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13
Q

do we measure height on a breathe in or out

A

out

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14
Q

what radiograph can be used to determine age of a child and why

A

left wrist

number of bones in wrist increases to 8 with age

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15
Q

what is growth velocity measured in and how often do we measure growth

A

cm per year
at least twice a year at 6 month intervals
height graph mirrors growth graph so use height

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16
Q

why is growth knowledge important for dentistry

A

BMI > average = increased risk of GA
coincide orthodontic treatment with puberty
must wait until growth complete before planning implants

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17
Q

what is CBT

A

cognitive behavioural therapy - talking therapy that can help you manage your problems by changing the way you think and behave

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18
Q

how can we talk to a child about their dental anxiety

A
  • ask them to scale their fear to MONITOR
  • ask them why they are scared and what they are scared of
  • if anything would make them feel better like a teddy, music, tv
  • childsense
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19
Q

why are the elderly less likely to seek dental assistance

A 
lack of ability to move
medical problems take more priority 
lack of help
lack of time
ignorance
dont see importance
social isolation
diseases/syndromes
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20
Q

what is domiciliary dentistry, breifly explain

A

dentistry for elderly where we go to their home
always need a nurse
can do simple procedures like fixing dentures and simple restorations

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21
Q

what must we have in a dental practice to allow elderly patients

A 
ramps
elevators if needed
disabled toilets 
Automatic doors
Banisters
good lighting 
not too cold
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22
Q

what does tooth loss in the elderly affect

A

denture stability and retention (and need of dentures)
reduced chewing capability
affecting aesthetics and social outgoingness
jaw registration

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23
Q

why is mandible resorption good and bad for elderly

A

good - if very high mandible, dentures have to be very thin and get midline fractures
bad - too resorbed and very poor stability of dentures

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24
Q

what is ageing

A

combination of biological, psychological and social processes that affect people as they grow older being dissociation from society, reduction in strength, mobility and ability to act

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25
Q

why is age a high risk factor for tooth loss

A

cumulative disease
failing restorations
polypharmacutical side effects like xerostomia
reduced manual dexterity for cleaning teeth

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26
Q

what is an age strata

A

group of ages in which people have share similar social rights and responsibilities e.g. elderly pensioners, school kids, university, at work

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27
Q

what is an age cohort

A

group of people who have similar experiences due to being born in a similar time

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28
Q

with older patients, what may they have experienced? how has dentistry changed

A

new laws and rules, now more preventative and patient centred
decreased prevalence of caries
now more analgesics and pain relief without gas
better restorations (less amalgam unlike the heavy metal generation with lots of amalgam)

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29
Q

what is the disengagement theory and what causes it

A

as we age, we disengage and distance from society
less contact and communication with outside world and society
reduced mobility, confidence, mental capacity

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30
Q

what is the structured dependency theory and how has this changed

A

idea that with age we are forced into certain choices e.g. retirement, less social interaction and to be dependant on the state leading to poverty
this has now changed and people can decide when they want to retire

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31
Q

what are barriers to elderly dental health

A

lack of domically dentistry
inability to get to a dentist due to lack of support or mobility or mental capacity
lack of equipment in care homes
reduced manual dexterity so struggle brushing teeth

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32
Q

what is the third age of life

A

reduced reasonability like jobs and child rearing

having less to do

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33
Q

what is the fourth age of life and how does this impact on dentistry

A

when the patient feels as if they are trapped in a body that is breaking down
try to fix their body
want new teeth to look useful therefor more dentures

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34
Q

what is critical gerontology

A

works in favour of elderly who feel left out of the ‘perfect white smile’ act
looks at the effect of advertising the perfect white smile and looks at effects of medical development on the elderly
elderly consideration

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35
Q

what is cultural gerontology

A

focus on the role of culture on elderly and how it affects their lives

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36
Q

what types of disorders of growth can there be

A

Congenital

Aquired

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37
Q

what are labile cells and give some examples

A

cells constantly dividing

GI cells, skin cells, bone marrow

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38
Q

what is a permanent cell and give an example

A

a cell that will no longer divide

neuron cells

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39
Q

what happens if we put stress on a labile cell

A

hyperplasia

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40
Q

what happens if e put stress on a permanent cell

A

hypertrophy

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41
Q

what are quiescent cells

A

cells currently not dividing but if stress is put on them they will divide

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42
Q

what is a hamartoma

A

an overgrowth of a section of tissue within growing tissue
benign tumour
stops growing when the tissue stops growing

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43
Q

what type of overgrowth is an odontoma

A

hamartoma

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44
Q

what are pigmented nevi and what type of growth is this

A

moles

hamartoma - benign stops growing when individual stops growing

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45
Q

what is reactive/adaptive hyperplasia

A

overgrowth caused by a stimulus

will stop when the stimulus is removed

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46
Q

what ion is needed for thyroid growth and production

A

iodine

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47
Q

when do we get adaptive hyperplasia

A

puberty/growth
pregnancy
pathology

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48
Q

explain why thyroid hyperplasia occurs

A

reduced iodine reduced thyroid production
negative feedback to pituitary gland
leads to increased production of labile thyroid cells –> overproduction

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49
Q

where do we get pure hypertrophy (3)

A

muscle growth under stress
smooth muscle in pregnancy
cardiac muscle under high blood pressure

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50
Q

what is the different between neoplasia and reactive hyperplasia

A

when the stimulus is removed:
hyperplasia stops
neoplasm keeps growing

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51
Q

what is the term for no growth atall

A

agenesis

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52
Q

what is aplasia

A

structure grows but not to full capacity -underdeveloped

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53
Q

if something is underveloped what is it called

A

aplasia

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54
Q

compare aplasia and hypoplasia

A

aplasia is undergrowth of something, underdeveloped

hypoplasia is full development but small

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55
Q

what is the term for an organ that has grown to full potential but is too small

A

hypoplasia

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56
Q

what is atrophy

A

full development but then decrease in size and number after growth

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57
Q

how does atrophy occur

A

increased cell apoptosis

reduced cell proliferation

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58
Q

what type of growth occurs in osteoporosis

A

atrophy - reducce in size/number of bone cells

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59
Q

what is generalized atrophy

A

getting smaller due to age

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60
Q

why does osteoporosis cause bone fracture

A

atrophy of trabecular bone - reduction i n thickness
atrophy of elastic cells reducing elasticity
reduction in strength
under stress, less resistance = fracture

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61
Q

when does atrophy occur in the dentition

A

with age and loss of teeth, the mandible resorbs (atrophy) due to lack of pressure on the bone

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62
Q

what can induce msucle/bone/nerve atrophy

A

lack of movement or use of the muscle/nerve

lack of use of nerve

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63
Q

what does idiopathic mean

A

random

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64
Q

what disease has idiopathic atrophy

A

Romberg’s disease produces hemifacial atrophy where the muscles on one side of the face occur

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65
Q

what is metaplasia

A

change in type of cell by differentiation

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66
Q

how does smoking cause metaplasia and what is its affect

A

smoking and heat vapour
metaplasia cause respiratory epithelium –> squamous epithelia with no cilia or mucous gland
Respiratory tract reduced ability to remove foreign bodies leading to mucous going into lungs reducing capacity to breathe causing coughing

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67
Q

what can metaplasia pre-dispose

A

cancer

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68
Q

what is dysplasia

A

abnormal cell type, differentiaiton and growth patterns - size, number

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69
Q

what is ectopia

A

normal tissue grows in the wrong site

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70
Q

what type of growth is it if the canine grows where the incisor should

A

ectopia

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71
Q

what type of growth would it be if the lateral incisor grew in the right place, fully developed but was too small

A

hypoplasia

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72
Q

what is a neoplasm

A

an overgrowth of tissue

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73
Q

what 3 defining characteristics of a neoplasm are there

A

Unco-cordinated tissue growth
Persists after the provoking stimulus is removed
Clonal: a single cell of origin

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74
Q

what is anaplasia

A

cannot tell what type of cell it is

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75
Q

what is a defining feature of malignant neoplasm

A

invasion of underlying tissue

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76
Q

what is metastasis

A

migration and spread of tumour to a distant part of body

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77
Q

what cells would we find in tumours

A

cancerous cells
fibroblasts
blood vessels (angiogenesis)
other structural cells

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78
Q

what differentiates benign and malignant growth pattern (4)

A

benign : expansion, encapsulated in tissue, localised, slow

malignant: invasion, not encapsulated, metastasis, more rapid but variable

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79
Q

what differentiates benign and malignant tumours in histology

A

benign: resembles tissue of origin, uniform cell shape and structure
malignant: does not resemble tissue of origin, nuclear pleomorphism

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80
Q

what is nuclear pleomorphism

A

variation in size and shape of cells - sign of malignancy

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81
Q

what clinical effects/implications differentiate benign and malignant tumours

A

benign: localised tumour, localised pressure, if removed = cured
malignant: localised and distant tumour, local pressure and effects, if removed possibly not cured

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82
Q

what are the two types of origin of tumour

A

epithelial

mesenchymal

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83
Q

what effects can tumours have on the body and function

A

put pressure on important parts of body e.g. brain
block lumens e.g. GI tract or blood vessels
alter function e.g. if in a gland

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84
Q

what could happen if a neoplasm got really big

A

it may cause extreme problems

may also cut off its own blood supply becoming necrotic

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85
Q

compare normal cancerous cells to normal cells

A 
have a less regular shape, larger and more quantity
bigger nucleus : cytoplasm ratio
loss of specialized features
disorganised arrangement of cells 
poorly defined boundaries
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86
Q

if a tumour moves with pressure, what does this tell us about the tumour and why

A

likely benign
if well encapsulated by connective tissue, not anchored to surrounding tissue
mobile on pressure

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87
Q

what is a tumour capsule made of

A

connective tissue of the immediate surrounding tissue of the tumour

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88
Q

what percent of tumours of mesenchymal and epithelial

A

mesenchymal : 10%

epithelial : 90%

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89
Q

what are epithelial cells derived from

A

epiderm, ectoderm and mesoderm

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90
Q

what classes as mesenchymal tissue

A

connective tissue, blood vessels, lymphatics

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91
Q

what is the name for a benign and malignant epithelial lining tumour

A

benign: papilloma
malignant: carcinoma

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92
Q

what is the name for a benign and malignant glandular epithelial tumour

A

benign: adenoma
malignant: adenocarcinoma

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93
Q

where is a colon adenocarcinoma likely to spread

A

liver

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94
Q

what does the name of mesenchymal cancer depend on

A

tissue of origin

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95
Q

what is the suffix of a benign mesenchymal cancer

A

‘oma’

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96
Q

what is the suffix of a malignant mesenchymal cancer

A

sarcoma

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97
Q

name some benign mesenchymal cancers with origin

A

osteoma - bone
myoma - muscle
lipoma - fat tissue
chondroma - cartilage

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98
Q

wat is the radiographic evidence of a osteosarcoma

A

‘burst’ of radiopacity with small fibres of bone

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99
Q

if we were to get cancer of a mole, what would this be

A

melanoma

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100
Q

what is a teratoma and what makes it different to any other cancer

A

cancer of germ cells - ovaries and testes
meiosis means it can take on any cell e.g. teeth
most malignant and mostly in testes

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101
Q

why do cancers arise

A 
bening - little evidence
malignant - inherited, environmental
-single point mutations
-free radicals
-DNA mutations in repair
-mutations in apoptosis e.g. BCL-2
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102
Q

what types of carcinogen can lead to malignancy

A

chemical
viral
physical
carcinogens

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103
Q

what are inherited cancer syndromes, what does this often occur in and how likely is it if we have this gene

A

single mutant genes like on tumour supressing genes
passed down through genetics
cause retinoblastoma and colon cancer
almost 100% likely to get cancer if this gene is present

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104
Q

what are familial clusters and what is a common example

A

clusters of family members all getting similar cancer
cause not known
premenopausal breast cancer with BRCA1/2 genes

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105
Q

how do we screen for premenopausal cancer

A

test for BRCA 1/2 gene
if they have a common mutation we can tell this pt is more likely to get cancer
BRCA 2 is worst incidence

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106
Q

what genetic factors lead to cancer

A

single mutant genes - inhertied cancer syndromes
familiar clusters of cancer
defective DNA - bad repair, apoptosis or replication

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107
Q

differentiate familial and inherited cancer

A

inherited is caused by a mutation on a single gene

familial is not caused by a change in 1 gene

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108
Q

what separates stellate reticulum from dental papilla

A

internal enamel epithelium - odontoblasts

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109
Q

what is hertwigs root sheath

A

where external and internal enamel epithelium join and proliferate to outline the roots

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110
Q

what is found within external and internal enamel epithelium and hat is its function and fate

A

stellate reticulum

provide nutrients for odontoblasts to form enamel prisms

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111
Q

what will dental papilla turn into

A

dentine

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112
Q

what is the cervical loop

A

where internal and external enamel epithelia meet to form hertwigs root sheath

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113
Q

what is the thin layer between odontoblasts and dentine

A

pre-dentine - The organic fibrillar matrix of the dentin before its calcification.

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114
Q

what is a pro-carcinogen

A

a protein that is metabolised to become an ultimate carcinogen

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115
Q

what is an ultimate carcinogen

A

a protein/chemical that directly causes cancer

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116
Q

what is a co-carcinogen

A

doesn’t cause cancer by itself

when in the presence of a carcinogen, amplifies the cancerous affect

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117
Q

what is the latent period of a tumour

A

the time from initiation to a clinical lesion

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118
Q

what are the 2 stages of chemical carcinogens

A

initiation - permanent DNA damage

promotion - proliferation of damaged DNA

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119
Q

what are some chemical and physical carcinogens

A

chemical:

  • nicotine
  • asbestos
  • alcohol

physical:

  • ionising radiation e.g. x-rays
  • radon gas
  • radioactive elements e.g. iodine –> thyroid cancer
  • UV light causes latent skin cell cancer
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120
Q

what skin cancers are cause sby UV light

A

squamous cell carcinomas
melanoma
basal cell carcinoma (most common)

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121
Q

how does HPV virus cause cancer and which cancer

A

over 50% of oropharyngeal cancers are caused by HPV
oropharyngeal carcinoma
attacks p53 tumour suppressor gene

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122
Q

how does ethanol cause cancer

A

co-carcinogen dissolves cigarette constituents into epithelium of mouth increasing cancer risk
pro-carcinogen as when metabolised, carcinogens are released causing direct cancer

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123
Q

what is a cancer of a gland

A

adenoma if benign

adenocarcinoma if malignant

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124
Q

give a few diseases that cause cancer

A

human papilloma virus HPV causes oropharyngeal carcinoma
Epstein-Barr Virus causes nasopharyngeal carcinoma
Hepatitis B/C

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125
Q

why is cancer more relevant in lower socioeconomic status

A

generally more smoking (class I)
more drinking (class I)
unhealthy eating e.g. more processed meats (Class II)
transfer of disease is more prone –> HPV, Epstein-Bar virus, Hepatitis B/C

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126
Q

what does De-Novo mean

A

cancer coming out of nowhere - no known cause

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127
Q

what is premalignancy and how do we spot these in the mouth

A 
a premalignant tumour, not yet causing cancer but a disruption in cell tissue that can be detected upon screening
red patches (erythroplakia) or white patches (leukoplakia)
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128
Q

how many bones are there in the head

A

28 excluding the hyoid bone

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129
Q

what is the head:body at birth and audlthood

A

1: 4 at birth
1: 8 at adulthood

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130
Q

compare intramembrnous bones and endochondrial bones

A

intramembranous bones grow by perioesteal remodelling

endochondral bones grow by cartilaginous replacement

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131
Q

what is the structure of the skull at birth and why

A 
cranial bones are lightly connected by soft membranous gaps called fontanelles 
1 anterior
1 posteiror
2 sphenoid
2 mastoid 
gives skull flexibility at birth
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132
Q

what is the adult skull split into

A

cranial vault
cranial base
nasomaxillary complex
mandible

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133
Q

when is the brain at full weight

A

11 years old

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134
Q

what % of brain weight is the brian at birth, 3 years, 7 years and 11 years

A

birth = 50%
3 years = 75%
7 years = 90%
11 years = 100%

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135
Q

why does the skull expand from birth

A

growth of interior brain

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136
Q

breifly, how does the skull develop to 18 years old

A

to early teens, sutures fuse

through adolescence; mandible protrudes, nasomaxillary complex matures

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137
Q

what is the function of the cranial vault

A

store and protect the brain

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138
Q

what bones make up the cranial base and how does it grow

A

frontal, ethmoidal, sphenoid, occipital, temporal

endochondral ossification

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139
Q

what are the cranial bones initially connected by

A

Fontanelles
sychondroses
cartilagenous connections of bone

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140
Q

whta is the fate of sychondroses

A

endochondral ossification

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141
Q

what bones make up the cranial vault starting anteriorly

A

frontal, ethmoid, sphenoid, temporal, parietal, occipital

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142
Q

which sychondroses is important for anterior posterior growth of the cranial base

A

spheno-occipital sychondroses

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143
Q

what is involved in the nasomaxillary complex

A

nose
maxilla
other small associated bones

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144
Q

what is the general growth of the nasomaxillary complex

A

maxilla moves down and anterior
Maxillary widens
nose protrudes
orbits move posterior

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145
Q

how and when does the maxilla widen and how is this relevant to dentistry

A

maxilla should widen during puberty
due to fusion of mid-palatal suture fusion
pre-puberty we can widen palate and maxilla before fusion of the suture if there is overcrowding/orthodontics

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146
Q

how does the mandible change shape with growth

A

increases in length and height
glenoid fossa is altered to be deeper
condyle grows by endochondral ossification
decreases in angle by 2-4 degrees

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147
Q

how does the mandibular condyle grow and how is this relevant to dentistry

A

with age the mandibular condyle grows in height
by endochondral ossification or secondary cartilage
if occlusion is too heavy, we can stimulate further cartilage growth at the condyle to loosen load on teeth
Explains sexual mandibular dimorphism

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148
Q

how is the rotational growth of the mandible relevant

A

with age the mandible rotates 2-4 degrees
can alter overbite causing class III occlusion
can alter OVD

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149
Q

what are growth sites

A

where the growth occurs e.g. bone surface

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150
Q

what are growth centres

A

growth sites that are independent and genetically controlled

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151
Q

why can we use growth of the face to determine age in young age

A

growth of mandible and maxilla occurs at similar rates to overall growth in young age

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152
Q

does the maxilla or mandible grow faster

A

maxilla

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153
Q

what can cause abnormal growth

A

congenital disorders - achondroplasia
acquired disorders
trauma
primary growth disorders

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154
Q

what is achondorplasia

A

congenital disorder leading to lack of cartilage in bone formation
no endochondral ossification
show limbs and long bones
large forehead but small skull

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155
Q

how common is cleft lip and palate and how does it occur

A

1 in 700

failure of fusion of palate sutures and lip sutures

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156
Q

what types of cleft lip and palate are there

A 
unilateral CLP = 40%
CL = 30%
bilateral CLP = 10%
CP = 10%
other = 10%
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157
Q

when does biological negative ageing start

A

after sexual maturity

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158
Q

what are the two biological theories of ageing

A

programmed:

  • biological hormones
  • telomeres on genes

non-programmed:

  • stochastic and cumulative disease
  • random cell damage and DNA
  • functional decline in systems
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159
Q

how do we know that ageing isn’t completely genetic

A

monozygotic twins with the same genes do not age the same

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160
Q

what types of disease are Hutchinson and Werner disease

A

accelerated growth

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161
Q

how does calorie intake affect ageing

A

malnutriton = poor growth

Okinawa have highest age but 40% reduction calorie intake to rest of population

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162
Q

how does mitochondrial dysfunction lead to ageing

A

leakage of electrons from electron transport system = less ATP
free electrons can form free radicals causing DNA alterations and cancer

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163
Q

what is a biological clock and how is it controlled

A

biological factor behind ageing
telomeres are sections of DNA at the end of chromosomes
every time the chromosome replicates the telomeres gets shorter
when telomere is used up this = senosence
cell continues in function but does not replicate

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164
Q

what is senescence

A

where the telomere of a chromosome has become so short that the cell will no longer divide but carry on in function
side affect of ageing

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165
Q

how do cancerous cells become imortal

A

use reverse transcriptase telomerase to add proteins back on telomerases to reduce senescence = continual proliferaiton
use proteins/transcirption factors like BCL-2 to prevent apoptosis

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166
Q

how may being active possibly increase age (3)

A

burn fat and sugar = less diabetes and obesity = less cancer

relationship between being active and longer telomeres = longer biological clock

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167
Q

how does smoking make us look older

A

chemicals in smoke increase metalloproteinase
breaks down collagen and reduce structure in skin
wrinkles form
give impression of ageing

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168
Q

what is stem cell exhaustion and how does it affect the body

A

reduction in the number of stem cells
reduced capacity to regenerate cells
bone marrow stem cell exhaustion leads to less immune cell production = worsened immune response

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169
Q

what is isometric growth

A

progressive proportional increase in size and function of all organs with time

170
Q

what is allometric growth

A

differences in the relative rates of growth between one part of the body and another

171
Q

what does the coronal suture separate

A

parietal (posterior) from frontal (anterior) bones

172
Q

what is the difference in growth anterior and posterior of the coronal suture

A

posterior is derived from mesoderm

anterior is derived from ectomesenchymoma from neural crest

173
Q

what is the first process of growth in Eco mesenchymal and mesodermal growth

A

condensation - coming together, coalescence, of cells to form dense cell groups

174
Q

which parts of the skull follow IMO and ECO

A

cranial vault and facial skeleton grow by IMO

cranial base and mandible grow by ECO

175
Q

what are the 2 fates of the condensed ecomesenchymal/mesodermal cells

A

will either differentiate into cartilage to then convert into bone - ECO
differentiate directly into bone IMO

176
Q

what is interstitial growth and where does it occur

A

cell division and matrix proliferation throughout structure - occurs in most organs

177
Q

what is appositional growth

A

directional growth - addition of material to existing surfaces (bone)

178
Q

differentiate growth of soft tissue and bone

A

soft tissue grows by interstitial growth - proliferation of cell and matrix throughout tissue
bones grow by directional appositional growth - addition of tissue onto existing surfaces (mostly excluding IMO)

179
Q

what is the growth pattern of ECO bone and IMO bone

A

ECO lays down cartilage by proliferation and then converts to bone - interstitial growth = longitudinal growth (long bones and cranial base)
IMO undergoes appositional growth with an increase of diameter of bone (cranial vault and facial skeleton)

180
Q

what are general (systematic) and local factors affecting bone growth

A

general:

  • nutrition and availability of calcium, vitamin D
  • hormones e.g. sex hormones, PTH, calcitronin
  • genetic influences

local:

  • Growth pattern (i.e. somatic, neural) - skeletal bones following shape of the body, bones follow neural patterns
  • Capsular matrices (enclosed tissues)- encasing bones follow their enclosed tissues (brain, eye sockets)
  • Periosteal matrices (muscle attachments, teeth) - influencing growth of bones
181
Q

when do fontanelles close

A

12-18 months after birth

182
Q

where does most postnatal cranial growth occur

A

facial skeleton and mandible/maxilla maturaiton

183
Q

why is the sphenoid-occipital sychondrose relevant to dentistry

A

relates to cranial lengthening by ECO of the cranial base
should continue until 18 but if premature to allow accommodation for 2nd and 3rd molars
can leave less space for wisdom teeth = impacted wisdoms

184
Q

what are the reasons for cranial base growth and how does this occur

A

lengthening
ECO of cranial base, mainly concerning the spheno-occipital sychondroses
allows accommodation for 2nd and 3rd molars
also increases cranium size to accommodate for increasing size of brain

widening
also increases cranium size to accommodate for increasing size of brain
allows correct positioning of TMJ with mandible

185
Q

Briefly explain the growth of the cranial vault

A

born with large fontanelles , fibrous membranes, between bones to allow flexibility for birth
12-18months post birth = fontanelles reduce by bones IMO but still fibrous attachments between bones = sutures
bones grow by IMO proportional to encapsulated brain following neural pathways
sutures ossify with maturity preventing any further growth of vault

186
Q

describe the growth of the facial skeleton

A

bones grow by IMO well into adulthood
mandible moves anterior and down by deposition and resorption = remodelling
nose extends and becomes more prominent
maxilla is widened by midpalate suture and is carried downwards by extension of nasal septum and orbits
sutures ossify e.g. midpalate suture

187
Q

explain growth of maxilla

A

IMO
bone resorbed on nasal aspect of palate and deposited on oral surface of palate translocating down
rapid deposition at tuberosities translocate maxilla forward
deposition is greater than resorption so growth as well as translocation

188
Q

explain growth of the mandible

A

mainly IMO
rapid ossification at ramus of mandible by IMO to position the condylar head in TMJ
secondary cartilage (not pharyngeal) is deposited on condyles allowing ECO lengthening of condyles
angle more inferiorly to allow occlusion of teeth

189
Q

which lip grows faster

A

lower

190
Q

compare embryological and developmental defects

A

E: evident at birth, may worsen with growth, more severe and cause problems with life
D: possibly not evident at birth, worsen with growth

191
Q

what is the most common craniofacial devlopmental defect

A

cleft lip and palate

1 in 680 births

192
Q

what affects on the pt does cleft lip and palate have

A

aesthetics
speech as the palate and lips play a strong role
hearing - palate has control over drainage from Eustachian tube
= glue ear = hearing aid or small tubes in tympanic membrane
dental abnormalities

193
Q

what dental problems does clef lip and palate cause and why

A

overcrowding due to lack of expansion of the maxilla = not enough space
Skeletal III occlusal relationship as mandible grows at faster rate to maxilla
high caries risk due to combination of dental anomolies

194
Q

what dental problems does clef lip and palate cause and why

A

overcrowding due to lack of expansion of the maxilla = not enough space
Skeletal III occlusal relationship as mandible grows at faster rate to maxilla
high caries risk due to combination of dental anomolies

195
Q

explain facial clefting and what dental representations would this include

A

where the right and left hemispheres of the brain fail to separate so the brain is one and this affects any midface features like the pituitary gland, eyes and nose
This is called Holoprosencephaly
3 front teeth, lack of smell

196
Q

at what age do prescriptions become free

A

65

197
Q

what NICE guideline covers oral health for elderly

A

48

provide oral and dental care in care homes

198
Q

what oral changes occur with old age

A

loss of teeth and heavy decay
bone resorption
tooth sclerosis causing reduced sensitivity
changes to oral mucosa becoming variably less or more flexible

199
Q

which bones grow by ECO and IMO

A 
ECO = most long bones in body, mandible and cranial base
IMO = cranial vault and facial skeleton and clavicle
200
Q

describe IMO

A

mesenchymal stem cells condense and differentiate into osteoblasts
lay down osteoid (non-mineralized bone matrix mainly collagen I and collagen V)
mineralize the osteoid
osteoblasts get trapped and become calcified = osteocytes and control calcium homeostasis and resorption
osteoclasts an osteoblasts remodel bone

201
Q

what are Haversian systems

A

unit of compact/cancellous bone

Rings of bone (osteon) with central blood vessels and nerve supply (harversian)

202
Q

what are the three phases of ECO

A

(ecto)mesenchymal cells differentiate into chondroblasts –> chondrocytes and lay down cartilage in miniature blueprint of bone
cartilage laid down in specific direction (appositional, length, or interstitial, diameter)
cartilage converted to bone by ossification

203
Q

what cells are involved in cartilage formation (3)

A

stem cells - ectomesenchymal or mesechymal
differentiate into chondroblast
mature into chondrocyte –> secrete cartilage matrix

204
Q

what 3 zones do we find in bones growing by ECO

A

proliferation zone: proliferating chondrocytes, forming ECM
hypertrophic zone: chondrocytes grow 5 fold, growth factors to stimulate angiogenesis
cartilage/bone interface: angiogenesis, mineralization of ECM and cartilage, apoptosis of chondrocytes

205
Q

what 3 things happen during the cartilage/bone interface of EMO

A

apoptosis of chondrocytes
angiogenesis blood vessel formation (for Haversian systems)
ossification and mineralization of cartilage matrix = bone formation

206
Q

compare the structure and position of osteoclasts and osteoblasts

A

osteoblasts: small, cuboidal, single nucleated cells found on bone surface
osteoclasts: large multinucleated cells found outside bone surface

207
Q

what 3 situations does remodelling occur

A

converting woven bone into cancellous bone
make new bone
break down existing bone

208
Q

compare bone resorption time and deposition time

A 
resorption = 3-4 weeks
deposition = 3-4 months
209
Q

compare bone fracture and tooth socket healing

A

bone fracture is IMO and ECO with haemastasis, callus formation, calcification, remodelling
tooth socket is only IMO, haemastasis, granulation tissue, woven bone deposition, remodelling

210
Q

does tooth socket healing occur by IMO or ECO

A

IMO

211
Q

explain bone remodelling

A

osteoclast precursor recruited
bone lining cells destroy some bone surface to expose ECM
osteoclast precursor –> osteoclast attaches to exposed ECM
digest bone tissue causing pits - howships lacunae
osteoclast apoptosis
osteoblast precursor recruited
osteoblast precursor –> osteoblast and lay down osteoid and mineralize in howships lacunae
osteoblasts turn into osteocytes (embedded in bone), bone lining cells or apoptosis

212
Q

what is a common IMO disorder

A

cleidocranial dystosis
1 in 1000000
affects gene acting on osteoblast and chondrocyte differentiation
reduced or absent clavicle, reduced devlopment of cranial vault and severe malloclusion and late eruption

213
Q

what are the dental and bodily affects of cleidocranial dysostosis

A 
affects gene acting on osteoblast and chondrocyte differentiation 
reduced or absent clavicle
reduced development of cranial vault 
severe malloclusion
late eruption
214
Q

explain a common ECO disorder

A

achondroplasia
affects the template cartilage formation of bone during initial ECO
reduces growth of all ECO bones being all skeletal bones and basocranium
flatter face
class III occlusion

215
Q

why do we get more cancer with age

A

worse cell turnover
reduced ability to fix DNA
accumulation of gene errors

216
Q

why is cerviacle cancer more prevelent in low income areas

A

less education
less vaccination
less screening

217
Q

what dietary/body factors have higher risk factors for cancer

A

alcohol
lack of fibre
processed red meats
body fatness

218
Q

How common is oral cancer, which sex is more likely and what are some high risk factors

A

8th most common cancer
men 3x more likely
obesity, smoking, alcohol, HPV, asbestos

219
Q

what is Ehlers-Danlos syndrome

A

Mutations in type V collagen, a regulator of type I collagen fibrillogenesis
poor wound healing, easy bleeding
Stretchy skin

220
Q

what is dry socket and what 2 types of osteitis are there for dry socket

A

early disruption of healing extraction socket

alveolar osteitis and fibrolytic osteitis - inflammation of alveolar socket bone

221
Q

what is rombergs disease

A

Romberg’s disease produces hemifacial idiopathic atrophy where the muscles on one side of the phase occur

222
Q

a patient has a random loss of function of half of their face and structure seems to be degrading. what are 2 differential causes

A

stroke
rombergs disease - hemifacial atrophy of the face
Bells Palsey

223
Q

how can cancer move

A

invasion of local tissue, down the path of least resistance e.g. nerves
metastasis by either:
-lymphatic system and get stuck in nodes forming secondary nodes here
-through blood vessels forming secondary nodes in liver, heart, brain
-seeding into cavities

224
Q

what abilities do tumour cells gain

A 
increased motility
alter adhesion molecules 
make poor basement membrane 
increase protease production or reduce inhibitors 
alter ECM
225
Q

how do carcinomas and sarcomas spread

A

Carcinomas (epithelial malignant) tend to spread through lymphatics and eventually the blood
Sarcomas (connective tissue malignant) spread through the blood

226
Q

what are some metastatic and non-metastatic effects and malignant cancer

A

metastatic:

  • haemorrage
  • pressure
  • obstruction
  • infection

non-metastatic:

  • Fever, anorexia and weight loss/cachexia
  • endocrine syndromes where tumour is overproducing hormones e.g. Cushings Syndrome metabolic effects upregulating cortisol or hypocalcaemia from increased Parathyroid Hormone action
  • neurological problems e.g. neuropathy
227
Q

what staging system is used to grade cancer at diagnsosis and what is it based on

A 
TNM histologically 
Tumour Size
Node number
Metastases (absent, present)
stage 1-4
228
Q

what is a common treatment of posterior tongue cancer

A

surgical dissection of tongue
removal of lymph nodes
splitting of jaw

229
Q

what are some side effects of cancer treatment

A 
tiredness
sickness
loss of hair
fatigue 
scarring
230
Q

what are some dental side effects of oral cancer treatment

A 
xerostomia if glands are affected 
struggle to eat and swallow
loss of hair 
sickness = erosion of teeth
If disectional - affects muscle and bone function
231
Q

what is IMRT

A

intensity mediated radiotherapy
localised, more precise radiation mainly used to avoid irradiation of the parotid gland during oral cancer treatment to prevent post operative xerostomia

232
Q

what can be used to avoid irradiation of parotid gland during oral cancer treatment

A

IMRT radiotherapy - intensity modulated radiotherapy

233
Q

how do tumour cells prevent T cell action

A

on their surface they have an atni-PD-L1 antigen o their surface which interferes with T cell action

234
Q

how does radiotherapy work

A

using very high doses of radiation to ionise and destroy cancer cells

235
Q

how does chemotherapy work

A

inhibitors growth factors used by tumour cells (and other cells) in blood stream to prevent further growth of tumours

236
Q

what are 2 syndromes that could be causes as a non-metastatic affect of a cancer in a gland

A

Cushing’s syndrome = increased cortisol levels = tumour overproducing cortisol in adrenal gland
Hypercalcemia = increased calcium = tumour overproducing PTH in PTG increasing osteoclast activity
Acromegaly or gigantism from pituitary gland neoplasm overproducing GH

237
Q

where is human growth hormone secreted

A

the pituitary gland

238
Q

where does the pituitary gland reside

A

pituitary fossa close to the optic chiasm

239
Q

what are some signs of a cancer in the pituitary gland

A

metastic effects: pressure build up against optic chiasm lead to loss of peripheral view and poor colour perception
non-metastic effects: increased human growth hormone and overall metabolism, acromegaly

240
Q

what is acromegaly and when does it occur

A

occurring in adulthood after epiphysial growth plates have closed
increased human growth hormone from anterior pituitary
lead to exaggerated soft and hard bones to become enlarged of secondary cartilage

241
Q

give two possible cancers that cause an increased hGH level

A

anterior pituitary adenoma or adenocarcinoma

lung adenocarcinoma for some reason differentiate into pituitary cells

242
Q

how does gigantism occur

A

increase in size of growth plates and activation of them before their closure + increased hGH

243
Q

what are some oral manifestations of acromegaly (growth hormone syndrome)

A

occurring in adulthood:

  • spacing between teeth
  • unusual changes to nose
  • enlarged lips
  • marks on inside of cheeks
244
Q

why must we identify acromegaly early on

A

it can lead to increased levels or not just bone but heart tissue
can lead to severe cardiac problems if untreated

245
Q

what stimulates release of growth hormone

A

growth hormone releasing hormone

from the hypothalamus

246
Q

what affects does growth hormone have on the body

A

direct e.g. stimulates directly to osteocytes
indirect acting on other glands e.g. liver to produce IGF-1
controls metabolism
maintains steady blood glucose levels

247
Q

what other hormone can we study instead of GH and why

A

look at IGF-1 released by liver ?(insluin like growth factor)
GH stimulates release of IGF-1 from liver for negative feedback
IGF-1 is less complicated and less fluctuating to study

248
Q

what is IGF-1 and why is it useful

A

insulin-like growth factor 1

stimulated release by GH and helps us study GH as it is less fluctuating

249
Q

which 2 glands does IGF-1 act on and how

A

inhibits production of GHRH from hypothalamus

inhibits release of GH from pituitary gland

250
Q

what affect does oestrogen have on growth

A

oestrogen stimulates release of growth hormone form pituitary gland
important for bone density growth e.g. osteoclast inhibition
affects on menstruation and growth in girls

251
Q

what affects does the time of puberty have on growth of girls

A

earlier the puberty initiation = smaller the woman

less gradual release of oestrogen so less gradual release of growth hormone

252
Q

what causes sexual mandibular dimorphism

A

women have more oestrogen and men have more androgens (testosterone)
oestrogen inhibits condylar growth (ECO)
testosterone activates condylar growth (ECO)
mens mandibles have a sharper angle than womens

253
Q

what affect do androgens have on growth

A

encourage lengthening and density increase of bones

254
Q

why does a woman have a shallower angle of mandible than a man

A 
sexual mandibular dimorphism 
women = oestrogen and men = testosterone = androgen
oestrogen inhibits condylar growth
testosterone excites condylar growth
leads to a different angle of mandible
255
Q

what are the functions of IGF-1

A

inhibits GH and GHRH
causes proliferation of myofibrils for muscle growth - hyperplasia
causes proliferation of chondrocytes for cartilage growth and bone growth

256
Q

what affect does thyroid hormone have on growth

A

thyroid hormone stimulates release of growth hormone
effects osteoblasts and chondrocytes
drives IGF-1 for growth

257
Q

where is the main acting site of IGF-1 on growth

A

epiphyseal plates
cartilage plates at ends of bones and stimulate chondrocyte proliferation
causing ECO bone lengthening (androgens also stimulate this)

258
Q

why are obese boys taller than not obese boys

A

obese boys eat more sugar and release more insulin

insulin acts on epiphyseal plates similar to insulin causing growth of ECO bones

259
Q

what is the main effect of hypothyroidism

A

shorter stature

due to less activation of GH and therefor less action of IGF-1 on epiphyseal plates

260
Q

what causes the 2 main peaks, and when, of IGF-1

A

Thyroid hormone peaks pre-puberty increasing IGF-1 release

Growth hormone is high during puberty causing increased IGF-1 release

261
Q

what affect do glucocorticoids have on growth and long term

A

increase stimulation of GHRH and GH in short term
decrease stimulation of GHRH and GH in long term
long term can cause glucose intolerance so should also go with insulin

262
Q

what are some side effects of glucocorticoids

A

osteoporosis due to ^ osteoclast and reduced osteoblast
immunosuppression due to reduced cytokine recruitment
diabetes by acting on GH and therefore IGF-1
Increased weight gain
Increased cortisol
Disrupted sleeping pattern

263
Q

what types of single point mutations can we get

A

change in amino acid = little affect
frameshift by addition/removal = large effect
introduce STOP codon leading to truncation

264
Q

how can mutation lead to truncation

A

introduce a STOP codon into DNA

leads to premature stopping of transcription

265
Q

what types of DNA mutation are there

A 
single base mutation
 -no change
 -frameshift
 -stop codon added
Gene amplifications
Chromosome translocation
266
Q

what are pro-oncogenes and where are they relevent

A

genes that release growth factors and increase expression of other genes
during a mutation of an pro-oncogene –> oncogenes this can lead to increased and uncontrolled proliferation

267
Q

what genes are likely to cause cancer if mutated

A

pro-oncogenes controlling expression of genes turn to oncogenes
tumour suppressor genes that inhibit proliferation
apoptosis genes like BCL-2
Cell cycle genes

268
Q

what is the two hit hypothesis

A

where the gene of one allele is damaged already/inherited

other gene sporadically gets mutated causing no healthy gene = cancer

269
Q

what is cephalometry and when is it used

A

radiographic imaging to measure planes of the skull. Can help determine treatment plan and growth

270
Q

what is the most common cephalograph

A

lateral

271
Q

at what point do we get a developed embryonic structure

A

3-4 weeks post conception

272
Q

what marks the posterior border of an embryo

A

mesenchymal somites up to the occipital somites

273
Q

what do we find at the top of an embryo from the lateral view

A

posterior - occipital somite’s
embryonic head with frontonasal process
anterior pharyngeal arches

274
Q

what do the somite develope into

A

vertebrae and ribs

275
Q

what do we find between the frontonasal process and pharyngeal arches and what will it develop into

A

stomodeum

mouth

276
Q

how many pharyngeal arches do humans have

A

4 with 5 and 6 forming the pericardiac sac (heart)

277
Q

what is the stomodeum and what membranes make it up

A

primitive mouth
between frontonasal process and pharyngeal arches
made by a very thin buccopharyngeal membrane of internal endoderm and external exoderm

278
Q

what is the buccopharyngeal membrane and when does it break down

A

in between the frontonasal process and pharyngeal arches we find the stomodeum
where the exoderm invaginates in to meet and create a membrane with the endoderm
this is called the buccopharyngeal membrane
breaks down 4 weeks after conception allowing opening into primitive gut

279
Q

where do we find the optic placode and what is its relevance

A

lateral of frontonasal process

thickened epithelium that will turn into the eyes

280
Q

what is the growth pattern of early pharyngeal arches

A

proliferate bilaterally towards the midline to join up and form sutures

281
Q

describe the structure of pharyngeal arches

A

surrounded externally by ectoderm with invaginations called clefts
surrounded internally by endoderm with invaginations called pouches
ecotomesenchyme in the middle
each phayrngeal arhc has associated nerve, artery, vein and cartilage

282
Q

why does it appear that the human embryo has 5 phayngeal arches

A

actually have 4

highest arch 1 is split in two: maxillary and mandibular

283
Q

which parts of the body does acromegaly affect

A

affects ECO epiphyseal plates after closure e.g. mid-age

e.g. mandible, nose and hands carry on growing

284
Q

what is the innervation of the 4 pharyngeal arches

A 
I = trigeminal (senosry) CNV
II = Facial (motor) CNVII
III = glossopharyngeal (tongue) CN IX
IV = Vagus (neck) CNX
285
Q

what genes control different proliferations in different pharyngeal arches

A

HOX genes found in rhombomeres

286
Q

explain the pathway of recurrent laryngeal nerves and why

A

branches of descending vagus nerve to come back to innervate right larnygeal muscles
right wraps around right subclavian artery
left wraps around the aortic arch (much more inferior)
because of HOX genes - pharyngeal arch 4 (vagus nerve) was is very close proximity to cardiac bulge
through devolvement and evolution, became further apart but the connection never changed

287
Q

what muscles do the pharyngeal arches innervate

A

I: CNV = muscles of mastication, suprahyoids, tensor veli palatini
II: CNVII = muscles of facial expression (orbicularis oris/occuli, metalis), some suprahyoids, stpaedius
III: CNIX = stylopharyngeous
IV: CNX = pharyngeal constrictors, soft and hard palate

288
Q

what cartilages come from which pharyngeal arches

A

I: meckels cartilage - teeth, incus, malleus
II: Stapes, Styloid process and ligament and Greater cornu of hyoid
III: majority of hyoid
IV: thyroid

289
Q

how does the ear form embryologically

A

the first pharyngeal cleft (ectoderm) invaginates into Eco mesenchyme to form the external auditory meatus
the first pharyngeal pouch (endoderm) invaginates into Eco mesenchyme to form the Eustachian tube
membranes meet to form the tympanic membrane

290
Q

what forms from the pharyngeal pouches - endoderm

A

I: eustachian tube to meet ectoderm to form tympanic membrane
II: parotid gland cells
III: inferior parathyroid cells
IV: superior parathyroid cells
V: thyroid cells that produce thyrocalcitonin

291
Q

how do we know the maxillary and mandibular pharyngeal arch are part of the same phayrngela arch

A

both innervated by the same nerve: CNV therefor due to HOX genes, same arch

292
Q

when does the first pharyngeal arch separate into Mn and Mx

A

4 weeks post conception

293
Q

what are the two reaons why it is important that the buccophayrngeal membrane breaks

A

to allow entrance ito the primitive gut

to separate nose and mouth

294
Q

how and when does the nose and primary palate start to form

A

nasal placodes invaginate into ectomesenchymoma on the frontonasal process at roughly 4 weeks post conception
cells proliferate around nasal placode causes medial/lateral nasal processes
the lower part of the invaginated nasal cavity is the primary palate anteriorly and posteriorly is the oronasal membrane

295
Q

what do nasal placode cells eventually turn into

A

oldfactory epithelium

296
Q

how does the primary palate form

A

invagination of nasal placodes into ectomesenchyme to cause nasal pits
lower border of this is anteriorly the primary palate and posteriorly the oronasla membrane
oronasal membrane breaks down causing a communication leaving only the anterior primary palate

297
Q

describe the growth of the maxillary process of the first pharyngeal arch

A

2 pairs of processes grow medially from the maxillary process; palatine (inferior) and tectoseptal (superior)
The Tectoseptal processes grow horizontally to meet at the midline (forming structures of the base of the skull) and then proliferate inferiorly to form the nasal septum
The palatine extends inferiorly on the lateral borders of the tongue. They then proliferate laterally to fill up a lot of the embryonic mouth.
The denser part of the palatine process has more proliferation and ECM.

298
Q

what two processes grow from the maxillary process and how do they grow

A 
Tectoseptal superiorly proliferates medially to meet at the midline and form the base of skull. They then row inferiorly at the midline to form the nasal septum
Palatine proccess (inferior) grows inferiorly down the latera; borders of the tongue and then proliferate laterally to fill the primative mouth
299
Q

what factor is released, and by what, for growth of the palate and what would a deficency in this lead to

A

FGF10
excreted by the ectomesenchyme
cleft palate

300
Q

what happens to the embryonic head at 8 weeks (explain why palatal elevation occurs(3))

A

The embryo develops a cervical flexure (only having one spinal flecture beforehand keeping the head close to the heart), lifting the head away from the cardiac bulge
The mandible widens allowing the tongue to drop into the floor of the mouth and create more superior space for developing palate
The palatal processes now have no restraint and elevate into a horizontal position above the tongue
=palatal elevation

301
Q

at what stage do the palatal processes meet

A

10 weeks post conception

302
Q

what fusion occurs at week 10 of embryonic stage (3)

A

palatine processes fuse:
together
with primary palate
with nasal septum

303
Q

what controls, and how does, fusion of maxillary processes at week 10

A

ectoderm cannot fuse with other ectoderm to releass Msx1 transcription factor
ectomesenchyme releases apoptotic factor in response, BMP4 and BMP2, to break down peripheral ectoderm
exposing underlying ectomesenchyme from middle outwards
this can fuse together in 2 weeks

304
Q

when should palatine fusion have occured

A

week 12

305
Q

what factors and proteins are released during fusion of palatine processes

A

when ectoderm is in close proximity, it releases the transcription factor Msx-1 to ectomesenchyme
ectomesenchyme gene BMP2 and BMP4 are upregulated and secreted to cause apoptosis of ectoderm
allows continuity between ectomesenycme and fusion over 2 weeks
FGF10 is kept high for proliferation of palatine processes and meet and fuse

306
Q

what derives the different part of the palate and at how many week post conception do they occur

A 
primary palate (upper anterior 1 and 2) from the anterior oronasal membrane invagination of frontonasal process 6 weeks
secondary palate from fusion of maxillary palatine process 12 weeks
307
Q

what is the evolutionary advantage of the palate

A

allows us to breathe and masticate at the same time

308
Q

what forms the borders of the mouth during embryological growth

A

fusion of the maxillary and mandibular processes

309
Q

during week 12-15 what can we see occurring in the palate (2)

A

anterior 2/3 invaded by bone

posterior 1/3 invaded by muscles of arch 4 (CNX)

310
Q

what causes cysts at the midline palate

A

fusion of palatal processes and nasal spine can leave remnant of epithelium
can eventually form epithelium bound cysts

311
Q

what causes the protrusion of the nose (2)

A

proliferation of the maxillary process and frontonasal process compresses the nose anteriorly
the anterior movement of the orbit and eyes make the midline features narrower

312
Q

what is macrostomia

A

larger macro, mouth stomia

wider mouth caused by failure of fusion of the maxillary and mandibular processes of pharyngeal arch 1

313
Q

what pregnancy factors can lead to clefts

A

alcohol
smoking
folic acid deficiency

314
Q

what causes a unilateral cleft lip and palate

A

failure of fusion between one side of the maxillary palatine process and the primary palate

315
Q

what causes a midline cleft palate

A

failure of the fusion between the 2 maxillary palatine processes

316
Q

what can cause cleft palate to occur

A

smoking, folate deficiency and alcohol during pregnancy (1st trimester - growth)
genetic mutations of the factors for fusion Msx-1, BMP2 and BMP4
very rare inherited genes on the X chromosome

317
Q

what mutaitons might lead to cleft lip and palate

A

transcription factor Msx-1 release by ectoderm

apoptotic factor BMP2 and BMP4 released by ectomesenchyme

318
Q

what forms the upper lip

A

merging of the medial walls of the nasal cavity and palatine processes of pharyngeal arch 1

319
Q

what causes cleft lip

A

fusion of the medial walls of the nasal cavity and the maxillary palatine process

320
Q

differentiate cleft lip from clef palate

A

cleft lip is the failure of fusion of the medial nasal processes and the maxillary process
left palate is the failure of fusion of the palatine shelves

321
Q

what is it called when our population is ageing and getting more disease

A

demographic shift

322
Q

what are some accelerated growth disorders

A

Wreners Syndrome

Hutchinsons Disease

323
Q

what are the social and medical models for disability

A

The medical model: Disability refers to the activity limitations that result in one or more chronic conditions.
The social model: disability is something produced by society through ‘disabling structures’ and ‘disabling societies’.

324
Q

compare impairments and disabilities

A

Impairment: any loss or abnormality of psychology, physiology or anatomical structures or function
Disability: restriction or lack resulting from an impairment which prevents ability to perform abilities.

325
Q

what is a handicap

A

a disadvantage in life to the pt due to an impairment or disability that limits fulfilment of a role

326
Q

why is the medical model of disability flawed and what should replace this and why

A

the patient becomes the problem e.g. cannot walk up stairs
social model shows disability is driven through social models e.g. should have rams in place for people that cannot walk up stairs

327
Q

how do dental practices bring in handicaps

A

wheelchair users cannot sit in the chair or get up stairs

328
Q

why might dentine sensitivity be classed as a disability

A

this is an impairment on a patient as it is an abnormality in physiology
this impairment causes discomfort and can alter how people live their life therefore is a disability

329
Q

histologically, what is found lateral to the Meckel’s cartilage in normal embryonic development

A

condensing ectomesenchymal cells into the mandible bone

330
Q

what is woven bone

A

immature bone with disordered matrix (high collagen III)

331
Q

what is the shape and function of osteocytes

A

stellate shaped
found within bone and their processes detect mechanical stimulus
if under pressure, they maintain bone density. If press is lost, they stimulate osteoclastic activity

332
Q

what proteins are rich at reversal lines

A

Sialoprotein and Osteopontin

333
Q

how can we identify reversal lines and what are they

A

dark blue lines
representing bone remodelling - changing from osteoclastic to osteoblastic activity
high in sialoprotein and osteopontin

334
Q

when do we get bone remodelling of alveolar bone (3)

A

exfoliation of teeth and changing alveolar socket
Orthodontic treatment artificially causing bone remodelling
when the tooth is lost and alveolar bone resorbs

335
Q

what would we see on a Pagets Disease pt histological bone

A

lots and lots of reversal lines

336
Q

what are the 5 zones of a ECO transition

A

hyaline cartilage progenitor cells
proliferative zone: cells proliferate, nuceli re-aranged and stacks of cells form
hypo trophic zone: nuclei become further apart separated by a white matrix. Chondrocytes then die
osteogenic zone: matrix infiltrated by blood vessels, osteoblasts and osteoclasts to mineralize and remodel cartilage
bone zone

337
Q

what is the spheno-occipital sychondroses and why is it special/important. Which disease affects this

A

the growth plate of hyaline cartilage between sphenoid bone and occipital bone
special as it has a growth plate on either side so can grow in both directions
important for bone lengthening
achondroplasia affects this plate and reduces length of skull

338
Q

which bone do we find the magnum foramen in

A

occipital bone of cranial base

339
Q

what age does palatal elevation occur

A

8 weeks

340
Q

what age does palatal elevation occur

A

8 weeks

341
Q

how long can separation anxiety affect a child

A

from 18 months to 5 years

342
Q

at what age can a baby start to understand simple words and turn toward sound

A

6 months

343
Q

what happens to a baby at age 6 months

A 
can sit by them self
curious and puts things in mouth
crys when left by parent
turns toward sound
understands simple words
344
Q

at what age can a baby start to wlak

A

12-18months

345
Q

what happens at 12-18months

A

can start to walk
throws toys
easily distressed
enjoys watching TV and understands their name
can do simple instructions like wave and help with routines e.g. collect nappy

346
Q

at what age can a baby recognise themselves in a picture

A

2 years

347
Q

what happens at 24 months old

A

walk up and down stairs
recognise themself in pcitures
understand 200 words
easily frustrated

348
Q

what changes occur from 2years old to 5 years old

A 
able to hop skip and jump
much broader language
confuse fact with fiction
play with others and help others when distressed 
understands jokes
likes stories
349
Q

what is a schema

A

unit of knowledge

used to measure a persons understanding of the world

350
Q

compare assimilation and accommodation of knowledge

A

assimilation is bringing in new knowledge to a body of knowledge
accommodation is adjusting the body of knowledge to add knowledge inconsistent to that already known

351
Q

what are the 4 phases of Piagets theory of development

A

Sensorimotor 0-2
pre-operational 2-7
concrete operational 7-12
formal operational >12

352
Q

explain the first phase of Piagets theory of devlopments

A

Sensorimotor 0-2
pre-operational 2-7
concrete operational 7-12
formal operational >12

Sensorimotor:
-Infants explore the world through their senses and applying their developing motor skills
Object permanence - understanding objects continue to exist when they cannot be seen e.i. looking for toys as opposed to not seeing a toy therefore not wanting a toy

353
Q

explain the second phase of Piagets theory of cognitive development

A

Sensorimotor 0-2
pre-operational 2-7
concrete operational 7-12
formal operational >12

Rapid development of language
Egocentrism – others see the world as they do
Development of symbolism - to make sense of the world e.g. bringing two objects together is represented symbolically by addition
Only operate physically cannot operate mentally

354
Q

explain the 3rd phase of Piagets theory of cognitive development

A

Sensorimotor 0-2
pre-operational 2-7
concrete operational 7-12
formal operational >12

Logical reasoning – real-world objects or events
Can begin to manipulate mentally
Empathise with others
Understanding that the physical properties of objects stay the same even though the appearance might change (can’t do with hypothetical objects)

355
Q

explain the 4th phase of Piagets theory of cognitive development

A

Sensorimotor 0-2
pre-operational 2-7
concrete operational 7-12
formal operational >12
Need exposure to principles of scientific thinking to reach this stage
Abstract reasoning – think and reason about hypothetical objects or events (take a mental representation and reason about them)
Future and health are difficult concepts to grasp

356
Q

why is there little point in telling a child health benefits of toothbrushing until the age of 12

A

age of 12 the child enters the fourth stage of Paigets theory of cognitive development: functional operational
able to grasp future concepts

357
Q

what are some faults with paigets theory of cognitive development

A

children progress at different rates
doesn’t account for disabilities
doesn’t account for different cultural upbringings

358
Q

Explain functional operational Ego-Centralism and how it affects life

A

young people above age of 12 believe others are as preoccupied with their appearance and actions as they are themselves – may feel as if they are the only one in the situation they are in.
They construct and react to an ‘imaginary audience’ where they are the centre and focus of attention – this audience can be very critical and negative, affecting mental health and self-consciousness.
They also believe in the uniqueness of their own feelings and their own immortality (personal fable).
affects dentistry wanting to sort out bad breath or aesthetics of teeth
affects confidence, appearance,

359
Q

what is the term for a young person around the age of 12 that feels very unconfident, uncomfortable and awkward

A

functional operational ego-centrisism

360
Q

what is a developmental disorder

A

a disorder which affects 1 or more developmental domain

pt is outside of 2 SD of the mean

361
Q

what causes developmental disorders

A 
Postnatal infections like meningitis
Maternal smoking, alcohol and drugs
Genetic Factors
Malnutrition 
Social factors like income, lone parenting etc
362
Q

how do we adapt our actions around a toddler

A

speak high pitched
understanding if they cry
keep appointment very short low attention span
do not separate from parent
relate going to bed without brushing like going to be without changing a nappies

363
Q

how do we adapt our actions with a 3-4 year old

A

Considered potentially co-operative
Gain attention with lots of distraction
Let them ‘help you’ where possible
Use appropriate language (childrenese) - relate rotary instruments to motor cars
Short attention span so work steadily and avoid pauses
Respond with rewards like stickers or sugar free sweets

364
Q

how do we adapt our actions when working school age children

A

Usually have sufficient co-ordination to brush their own teeth and can follow ‘rules’ about oral care
Try and involve children in what you are doing - they want independence
Respond well to positive reinforcement
Use appropriate language and simple explanations, and encourage questions
Try to gage responsibility and understanding of the child. 75% of 8-13 year olds feel like they understand the treatment and would like to be more involved.

365
Q

how do we change our actions with a teenage patient

A

Very sensitive and embarrassed by criticism
Try to make their own decisions and should be seen without parents
Motivated by attractiveness and focus more on aesthetic than health

366
Q

what is an autism spectrum disorder

A

neurodevelopmental disorder with unknown aetiology
affects 1:100 children
4x more likely in males
accompanies with ADHD/Seizures and 50% with learning difficulties

367
Q

how do we adapt our actions with a autistic patient

A

Minimise waiting times
Simple language, short sentences and direct requests
Avoid metaphors, sarcasm and joking
Remember sensory overload (lights/noise in surgery and taste of materials) - provide tasteless toothpaste?
Distress = Anxious behaviours (repetitive movements/aggression)

368
Q

when does growth occur at its fastest rate and how fast?

A

2nd trimester of pregnancy

2cm a week

369
Q

how do we find BMI

A

mass divided by height squared

370
Q

what determines growth in infancy, childhood and teenage years

A 
infancy = nutrition
childhood = GH
teenage = sex hormones and GH
371
Q

give some determinants of growth

A 
nutritional deficency
malabsorption = coaeliac 
systemic disease = hypothyroid, hypopituitary, heart problems 
steroid excess
inherited = achondroplasia
372
Q

what can birth defects be divided into

A

single/isolated defects affecting only 1 system

multiple defects

373
Q

what can multiple defects of birth defects be further divided into

A

Associations: Combination of at least 3 anomalies that occur together but where there is no clear mechanism. e.g. vacteral
Sequences: Sequences of anomalies that lead onto each other e.g. Pierre-Robin Sequence. This leads to Breathing difficulties, Feeding difficulties, Cleft palate, Speech therapy, Dental care and possible learning disability.
Field complexes: Insult to a localised part of an embryo resulting in abnormalities in adjacent structures of disparate embryonic origin including underlying muscles, bones, vascular tissue and nerves.
Syndromes: signs and symptoms that run together, seemingly involved with the same cause

374
Q

what causes dons syndrome

A

trisomy 21

third copy of 21st chromasome

375
Q

what are some dental manifestations of Trisomy 21

A 
downsyndrome
Large, fissured tongue
Periodontal disease
Hypodontia
Microdontia
Enamel defects
Class 3 malocclusion due to maxillary retrognathia
376
Q

what causes dentinogenetic imperfecta

A

DSPP dentine sialophosphoprotein mutaiton that usually coats non-collagenous dentine proteins
affects the non-collagenous proteins of dentine

377
Q

how many people are affected by dentinogenesis imperfecta

A

1 in 6000-8000

378
Q

what are some sings and symptoms of dentinogenetic imperfecta

A 
Amber, grey to purplish discolouration
Pulpal Obliteration
Relatively bulbous crowns
Short narrow roots
Enamel may be lost following tooth eruption exposing soft dentine which wears rapidly
Normal mantle dentine
Affects primary > permanent definition
379
Q

what are some signs of osteogenesis imperfecta

A 
bone fragility (vertebral) 
Connective tissue disease with thin blood vessels (bruise easily)
Poor muscle
Blue sclera
Progressive hearing loss
380
Q

what causes osteogenesis imperfecta

A

inherited autosomal mutation of a collagen gene effecting the production/processing of collagen 1

381
Q

what are two possible causes of rickets

A

malnutrition - not taking in enough vitamin D inhibiting calcium/phosphate uptake
X-linked hypophosphotatemia - dominant X linked disruption in calcium/phosphate metabolism

382
Q

what are some oral manifestations of rickets (3)

A

Large pulp chambers
elongated pulp horns
Abscesses in the absence of caries

383
Q

there are abscesses in the absence of caries. what growth disorder can cause this

A

X-linked hypophsophatemia (rickets)

384
Q

which gene is affected by X-linked hypophosphatemia

A

FGF23 involved in metabolsim of phosphate and calcium

385
Q

what oral manifestations of cleidocranial dysplasia are there

A

Hypoplastic maxilla & zygoma
Delayed exfoliation of primary teeth.
Multiple unerupted teeth and associated cyst
We can see teeth in both arches are not in the correct alignment and the maxilla is much smaller than the mandible.

386
Q

why is there a mis-alignment of maxilla and mandible in cleidocranial dysplasia

A

affects IMO
mandible grows partially due to ECO however maxilla grows solely by IMO
Causes class III and wider mandible than maxilla

387
Q

what is the enamel organ

A

during tooth development this involved the internal dental epitheliaum (turn into ameloblasts), stellate reticulum (turns into enamel) and external dental epithelium (turn into odontoblasts)

388
Q

where does the IDE and EDE meet

A

cerviacle loop

389
Q

how does space for PDL to insert onto the cementum form

A

as epithelial root sheath grows it expands and form gaps in-between the epithelium called epithelial cell rests of mallasez
these gaps allow sharpeys fibres to insert onto the dentine

390
Q

what does the dental follicle differentiate into

A

cementoblasts

fibroblasts

391
Q

what is mantel dentine and why is it formed

A

pre-odontoblasts secrete dentine matrix before they are fully devloped
this dentine has higher ECM than collagen

392
Q

how mineralized is cementum

A

55%

393
Q

what is the order of eruption of primary teeth

A

ABDCE

394
Q

when does the crown of primary teeth start mineralizing

A

begin mineralizing 3-6/12 i.u
finish 3-12/12 i.u
erupt 6/12 - 24/12 i.u
root finished 18/12 - 13/12 i.u.

395
Q

when are primary crowns fully mineralized

A

begin mineralizing 3-6/12 i.u
finish 3-12/12 i.u
erupt 6/12 - 24/12 i.u
root finished 18/12 - 13/12 i.u.

396
Q

when do primary crowns erupt

A

begin mineralizing 3-6/12 i.u
finish 3-12/12 i.u
erupt 6/12 - 24/12 i.u
root finished 18/12 - 13/12 i.u.

397
Q

when is the root fully developed of primary teeth

A

begin mineralizing 3-6/12 i.u
finish 3-12/12 i.u
erupt 6/12 - 24/12 i.u
root finished 18/12 - 13/12 i.u.

398
Q

what is the order of eruption of the secondary teeth

A 
6
1
2
4
5
3
7
8
399
Q

how do we find the age of a tooths crown start, crown finish, crown erupt, root finish

A 
order - 1 = crown start
crown takes 3 years to fully form
further 3 years to fully erupt
further 3 years for root to finish 
disregarding 3s and 8s
400
Q

when does the secondary canine start devloping

A

age 2

401
Q

how long does the canines root take to form

A

6 years

402
Q

when does the crown start forming of wisdom teeth

A

12 years old

403
Q

which is the only tooth to erupt with a fully formed root

A

secondary canine

404
Q

when do mandibular erupt in relation to maxillary teeth

A

mandibular erupt 6 months before maxillary

405
Q

if the LL6 erupts at 6 years old, when should the LR6 and UR6 erupt

A

within 6 months

406
Q

what are the first secondary teeth to erupt

A

mandibular first molars

407
Q

what happens at 4 weeks post conception

A

buccopharyngeal membrane breaks down to stomodeum

first arch split into maxillary and mandibular process

408
Q

what happens at 5 weeks post conception

A

invagination of nasal placode

growth of nasal processes

409
Q

what happens at 6 weeks post conception

A

outgrowth of palatal processes and tectoseptal processes
primary palate formed
md fusion at midline

410
Q

what happens at 8 weeks post conception

A

tongue drops

palatine elevation

411
Q

what happens at 10 weeks post conception

A

fusion of palatine, primary palate and medial nasal processes starts

412
Q

what happens at 12 weeks post conception

A

fusion of processes ends

413
Q

what happens at 12-15 weeks post conception

A

differentiation of cells of the oral cavity

414
Q

what do we need for a dental ageing evaluation

A

OPT radiograph

415
Q

what are the disadvantages and advantages of dental ageing

A 
\+uses maturity of teeth to evaluate age
\+accurate
\+simple
\+corresponds strongly with chronological age 
\+non-invasive
  • radio wave exposure
  • based on data from white population
  • no 8s so only up to 15 years old
  • doesn’t take into account imperfectas
  • doesnt take into account hormone disorders
  • not ethnically generalisable
416
Q

how are teeth rated whilst doing dental ageing

A

A to H

A being not developed H being fully developed

417
Q

what is chronological age

A

years from birth

418
Q

what is biological age

A

based on transitional change in biological landmarks

419
Q

why do we do dental ageing

A

dental ageing corresponds strongly with chronilogical age
useful for forensics
estimating ages of children with no parents

420
Q

what is the hayflick limit

A

number of times a cell can divide before being senescent - telomeres

421
Q

is telomeres length/hayflick limit evolutionary or programmed ageing

A

evolutionary

422
Q

what type of disease is crouzons

A

craniosystenosis

mishapen head due to premature fusion of sutures causing brain to expand against formed skull

BDS 2 (13 decks)

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