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
2
Q
when are childrens rapid growths?
A
0-2 child growth
12-18 through puberty
steady growth in the middle
3
Q
when would we make a paediatric referal in terms of BMI/height
A
if in the <3 centile or >97 centile
4
Q
what does a baby 0-2yr old’s growth depend on
A
growth disorders / health
mothers health
nutrition
Placental efficiency
5
Q
what is the leading cause of growth suppression
A
chronic illness e.g. undiagnosed coeliac/malnutrition
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
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
8
Q
how do we estimate the height of a child
A
take a mid parental height = should be +-10 within this
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
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
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
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
13
Q
do we measure height on a breathe in or out
A
out
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
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
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
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
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
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
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
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
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
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
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
25
why is age a high risk factor for tooth loss
cumulative disease
failing restorations
polypharmacutical side effects like xerostomia
reduced manual dexterity for cleaning teeth
26
what is an age strata
group of ages in which people have share similar social rights and responsibilities e.g. elderly pensioners, school kids, university, at work
27
what is an age cohort
group of people who have similar experiences due to being born in a similar time
28
with older patients, what may they have experienced? how has dentistry changed
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)
29
what is the disengagement theory and what causes it
as we age, we disengage and distance from society
less contact and communication with outside world and society
reduced mobility, confidence, mental capacity
30
what is the structured dependency theory and how has this changed
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
31
what are barriers to elderly dental health
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
32
what is the third age of life
reduced reasonability like jobs and child rearing
| having less to do
33
what is the fourth age of life and how does this impact on dentistry
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
34
what is critical gerontology
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
35
what is cultural gerontology
focus on the role of culture on elderly and how it affects their lives
36
what types of disorders of growth can there be
Congenital
| Aquired
37
what are labile cells and give some examples
cells constantly dividing
| GI cells, skin cells, bone marrow
38
what is a permanent cell and give an example
a cell that will no longer divide
| neuron cells
39
what happens if we put stress on a labile cell
hyperplasia
40
what happens if e put stress on a permanent cell
hypertrophy
41
what are quiescent cells
cells currently not dividing but if stress is put on them they will divide
42
what is a hamartoma
an overgrowth of a section of tissue within growing tissue
benign tumour
stops growing when the tissue stops growing
43
what type of overgrowth is an odontoma
hamartoma
44
what are pigmented nevi and what type of growth is this
moles
| hamartoma - benign stops growing when individual stops growing
45
what is reactive/adaptive hyperplasia
overgrowth caused by a stimulus
| will stop when the stimulus is removed
46
what ion is needed for thyroid growth and production
iodine
47
when do we get adaptive hyperplasia
puberty/growth
pregnancy
pathology
48
explain why thyroid hyperplasia occurs
reduced iodine reduced thyroid production
negative feedback to pituitary gland
leads to increased production of labile thyroid cells --> overproduction
49
where do we get pure hypertrophy (3)
muscle growth under stress
smooth muscle in pregnancy
cardiac muscle under high blood pressure
50
what is the different between neoplasia and reactive hyperplasia
when the stimulus is removed:
hyperplasia stops
neoplasm keeps growing
51
what is the term for no growth atall
agenesis
52
what is aplasia
structure grows but not to full capacity -underdeveloped
53
if something is underveloped what is it called
aplasia
54
compare aplasia and hypoplasia
aplasia is undergrowth of something, underdeveloped
| hypoplasia is full development but small
55
what is the term for an organ that has grown to full potential but is too small
hypoplasia
56
what is atrophy
full development but then decrease in size and number after growth
57
how does atrophy occur
increased cell apoptosis
| reduced cell proliferation
58
what type of growth occurs in osteoporosis
atrophy - reducce in size/number of bone cells
59
what is generalized atrophy
getting smaller due to age
60
why does osteoporosis cause bone fracture
atrophy of trabecular bone - reduction i n thickness
atrophy of elastic cells reducing elasticity
reduction in strength
under stress, less resistance = fracture
61
when does atrophy occur in the dentition
with age and loss of teeth, the mandible resorbs (atrophy) due to lack of pressure on the bone
62
what can induce msucle/bone/nerve atrophy
lack of movement or use of the muscle/nerve
| lack of use of nerve
63
what does idiopathic mean
random
64
what disease has idiopathic atrophy
Romberg’s disease produces hemifacial atrophy where the muscles on one side of the face occur
65
what is metaplasia
change in type of cell by differentiation
66
how does smoking cause metaplasia and what is its affect
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
67
what can metaplasia pre-dispose
cancer
68
what is dysplasia
abnormal cell type, differentiaiton and growth patterns - size, number
69
what is ectopia
normal tissue grows in the wrong site
70
what type of growth is it if the canine grows where the incisor should
ectopia
71
what type of growth would it be if the lateral incisor grew in the right place, fully developed but was too small
hypoplasia
72
what is a neoplasm
an overgrowth of tissue
73
what 3 defining characteristics of a neoplasm are there
Unco-cordinated tissue growth
Persists after the provoking stimulus is removed
Clonal: a single cell of origin
74
what is anaplasia
cannot tell what type of cell it is
75
what is a defining feature of malignant neoplasm
invasion of underlying tissue
76
what is metastasis
migration and spread of tumour to a distant part of body
77
what cells would we find in tumours
cancerous cells
fibroblasts
blood vessels (angiogenesis)
other structural cells
78
what differentiates benign and malignant growth pattern (4)
benign : expansion, encapsulated in tissue, localised, slow
| malignant: invasion, not encapsulated, metastasis, more rapid but variable
79
what differentiates benign and malignant tumours in histology
benign: resembles tissue of origin, uniform cell shape and structure
malignant: does not resemble tissue of origin, nuclear pleomorphism
80
what is nuclear pleomorphism
variation in size and shape of cells - sign of malignancy
81
what clinical effects/implications differentiate benign and malignant tumours
benign: localised tumour, localised pressure, if removed = cured
malignant: localised and distant tumour, local pressure and effects, if removed possibly not cured
82
what are the two types of origin of tumour
epithelial
| mesenchymal
83
what effects can tumours have on the body and function
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
84
what could happen if a neoplasm got really big
it may cause extreme problems
| may also cut off its own blood supply becoming necrotic
85
compare normal cancerous cells to normal cells
```
have a less regular shape, larger and more quantity
bigger nucleus : cytoplasm ratio
loss of specialized features
disorganised arrangement of cells
poorly defined boundaries
```
86
if a tumour moves with pressure, what does this tell us about the tumour and why
likely benign
if well encapsulated by connective tissue, not anchored to surrounding tissue
mobile on pressure
87
what is a tumour capsule made of
connective tissue of the immediate surrounding tissue of the tumour
88
what percent of tumours of mesenchymal and epithelial
mesenchymal : 10%
| epithelial : 90%
89
what are epithelial cells derived from
epiderm, ectoderm and mesoderm
90
what classes as mesenchymal tissue
connective tissue, blood vessels, lymphatics
91
what is the name for a benign and malignant epithelial lining tumour
benign: papilloma
malignant: carcinoma
92
what is the name for a benign and malignant glandular epithelial tumour
benign: adenoma
malignant: adenocarcinoma
93
where is a colon adenocarcinoma likely to spread
liver
94
what does the name of mesenchymal cancer depend on
tissue of origin
95
what is the suffix of a benign mesenchymal cancer
'oma'
96
what is the suffix of a malignant mesenchymal cancer
sarcoma
97
name some benign mesenchymal cancers with origin
osteoma - bone
myoma - muscle
lipoma - fat tissue
chondroma - cartilage
98
wat is the radiographic evidence of a osteosarcoma
'burst' of radiopacity with small fibres of bone
99
if we were to get cancer of a mole, what would this be
melanoma
100
what is a teratoma and what makes it different to any other cancer
cancer of germ cells - ovaries and testes
meiosis means it can take on any cell e.g. teeth
most malignant and mostly in testes
101
why do cancers arise
```
bening - little evidence
malignant - inherited, environmental
-single point mutations
-free radicals
-DNA mutations in repair
-mutations in apoptosis e.g. BCL-2
```
102
what types of carcinogen can lead to malignancy
chemical
viral
physical
carcinogens
103
what are inherited cancer syndromes, what does this often occur in and how likely is it if we have this gene
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
104
what are familial clusters and what is a common example
clusters of family members all getting similar cancer
cause not known
premenopausal breast cancer with BRCA1/2 genes
105
how do we screen for premenopausal cancer
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
106
what genetic factors lead to cancer
single mutant genes - inhertied cancer syndromes
familiar clusters of cancer
defective DNA - bad repair, apoptosis or replication
107
differentiate familial and inherited cancer
inherited is caused by a mutation on a single gene
| familial is not caused by a change in 1 gene
108
what separates stellate reticulum from dental papilla
internal enamel epithelium - odontoblasts
109
what is hertwigs root sheath
where external and internal enamel epithelium join and proliferate to outline the roots
110
what is found within external and internal enamel epithelium and hat is its function and fate
stellate reticulum
| provide nutrients for odontoblasts to form enamel prisms
111
what will dental papilla turn into
dentine
112
what is the cervical loop
where internal and external enamel epithelia meet to form hertwigs root sheath
113
what is the thin layer between odontoblasts and dentine
pre-dentine - The organic fibrillar matrix of the dentin before its calcification.
114
what is a pro-carcinogen
a protein that is metabolised to become an ultimate carcinogen
115
what is an ultimate carcinogen
a protein/chemical that directly causes cancer
116
what is a co-carcinogen
doesn't cause cancer by itself
| when in the presence of a carcinogen, amplifies the cancerous affect
117
what is the latent period of a tumour
the time from initiation to a clinical lesion
118
what are the 2 stages of chemical carcinogens
initiation - permanent DNA damage
| promotion - proliferation of damaged DNA
119
what are some chemical and physical carcinogens
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
120
what skin cancers are cause sby UV light
squamous cell carcinomas
melanoma
basal cell carcinoma (most common)
121
how does HPV virus cause cancer and which cancer
over 50% of oropharyngeal cancers are caused by HPV
oropharyngeal carcinoma
attacks p53 tumour suppressor gene
122
how does ethanol cause cancer
co-carcinogen dissolves cigarette constituents into epithelium of mouth increasing cancer risk
pro-carcinogen as when metabolised, carcinogens are released causing direct cancer
123
what is a cancer of a gland
adenoma if benign
| adenocarcinoma if malignant
124
give a few diseases that cause cancer
human papilloma virus HPV causes oropharyngeal carcinoma
Epstein-Barr Virus causes nasopharyngeal carcinoma
Hepatitis B/C
125
why is cancer more relevant in lower socioeconomic status
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
126
what does De-Novo mean
cancer coming out of nowhere - no known cause
127
what is premalignancy and how do we spot these in the mouth
```
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)
```
128
how many bones are there in the head
28 excluding the hyoid bone
129
what is the head:body at birth and audlthood
1: 4 at birth
1: 8 at adulthood
130
compare intramembrnous bones and endochondrial bones
intramembranous bones grow by perioesteal remodelling
| endochondral bones grow by cartilaginous replacement
131
what is the structure of the skull at birth and why
```
cranial bones are lightly connected by soft membranous gaps called fontanelles
1 anterior
1 posteiror
2 sphenoid
2 mastoid
gives skull flexibility at birth
```
132
what is the adult skull split into
cranial vault
cranial base
nasomaxillary complex
mandible
133
when is the brain at full weight
11 years old
134
what % of brain weight is the brian at birth, 3 years, 7 years and 11 years
birth = 50%
3 years = 75%
7 years = 90%
11 years = 100%
135
why does the skull expand from birth
growth of interior brain
136
breifly, how does the skull develop to 18 years old
to early teens, sutures fuse
| through adolescence; mandible protrudes, nasomaxillary complex matures
137
what is the function of the cranial vault
store and protect the brain
138
what bones make up the cranial base and how does it grow
frontal, ethmoidal, sphenoid, occipital, temporal
| endochondral ossification
139
what are the cranial bones initially connected by
Fontanelles
sychondroses
cartilagenous connections of bone
140
whta is the fate of sychondroses
endochondral ossification
141
what bones make up the cranial vault starting anteriorly
frontal, ethmoid, sphenoid, temporal, parietal, occipital
142
which sychondroses is important for anterior posterior growth of the cranial base
spheno-occipital sychondroses
143
what is involved in the nasomaxillary complex
nose
maxilla
other small associated bones
144
what is the general growth of the nasomaxillary complex
maxilla moves down and anterior
Maxillary widens
nose protrudes
orbits move posterior
145
how and when does the maxilla widen and how is this relevant to dentistry
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
146
how does the mandible change shape with growth
increases in length and height
glenoid fossa is altered to be deeper
condyle grows by endochondral ossification
decreases in angle by 2-4 degrees
147
how does the mandibular condyle grow and how is this relevant to dentistry
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
148
how is the rotational growth of the mandible relevant
with age the mandible rotates 2-4 degrees
can alter overbite causing class III occlusion
can alter OVD
149
what are growth sites
where the growth occurs e.g. bone surface
150
what are growth centres
growth sites that are independent and genetically controlled
151
why can we use growth of the face to determine age in young age
growth of mandible and maxilla occurs at similar rates to overall growth in young age
152
does the maxilla or mandible grow faster
maxilla
153
what can cause abnormal growth
congenital disorders - achondroplasia
acquired disorders
trauma
primary growth disorders
154
what is achondorplasia
congenital disorder leading to lack of cartilage in bone formation
no endochondral ossification
show limbs and long bones
large forehead but small skull
155
how common is cleft lip and palate and how does it occur
1 in 700
| failure of fusion of palate sutures and lip sutures
156
what types of cleft lip and palate are there
```
unilateral CLP = 40%
CL = 30%
bilateral CLP = 10%
CP = 10%
other = 10%
```
157
when does biological negative ageing start
after sexual maturity
158
what are the two biological theories of ageing
programmed:
- biological hormones
- telomeres on genes
non-programmed:
- stochastic and cumulative disease
- random cell damage and DNA
- functional decline in systems
159
how do we know that ageing isn't completely genetic
monozygotic twins with the same genes do not age the same
160
what types of disease are Hutchinson and Werner disease
accelerated growth
161
how does calorie intake affect ageing
malnutriton = poor growth
| Okinawa have highest age but 40% reduction calorie intake to rest of population
162
how does mitochondrial dysfunction lead to ageing
leakage of electrons from electron transport system = less ATP
free electrons can form free radicals causing DNA alterations and cancer
163
what is a biological clock and how is it controlled
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
164
what is senescence
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
165
how do cancerous cells become imortal
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
166
how may being active possibly increase age (3)
burn fat and sugar = less diabetes and obesity = less cancer
| relationship between being active and longer telomeres = longer biological clock
167
how does smoking make us look older
chemicals in smoke increase metalloproteinase
breaks down collagen and reduce structure in skin
wrinkles form
give impression of ageing
168
what is stem cell exhaustion and how does it affect the body
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
169
what is isometric growth
progressive proportional increase in size and function of all organs with time
170
what is allometric growth
differences in the relative rates of growth between one part of the body and another
171
what does the coronal suture separate
parietal (posterior) from frontal (anterior) bones
172
what is the difference in growth anterior and posterior of the coronal suture
posterior is derived from mesoderm
| anterior is derived from ectomesenchymoma from neural crest
173
what is the first process of growth in Eco mesenchymal and mesodermal growth
condensation - coming together, coalescence, of cells to form dense cell groups
174
which parts of the skull follow IMO and ECO
cranial vault and facial skeleton grow by IMO
| cranial base and mandible grow by ECO
175
what are the 2 fates of the condensed ecomesenchymal/mesodermal cells
will either differentiate into cartilage to then convert into bone - ECO
differentiate directly into bone IMO
176
what is interstitial growth and where does it occur
cell division and matrix proliferation throughout structure - occurs in most organs
177
what is appositional growth
directional growth - addition of material to existing surfaces (bone)
178
differentiate growth of soft tissue and bone
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
what is the growth pattern of ECO bone and IMO bone
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
what are general (systematic) and local factors affecting bone growth
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
when do fontanelles close
12-18 months after birth
182
where does most postnatal cranial growth occur
facial skeleton and mandible/maxilla maturaiton
183
why is the sphenoid-occipital sychondrose relevant to dentistry
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
what are the reasons for cranial base growth and how does this occur
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
Briefly explain the growth of the cranial vault
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
describe the growth of the facial skeleton
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
explain growth of maxilla
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
explain growth of the mandible
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
which lip grows faster
lower
190
compare embryological and developmental defects
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
what is the most common craniofacial devlopmental defect
cleft lip and palate
| 1 in 680 births
192
what affects on the pt does cleft lip and palate have
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
what dental problems does clef lip and palate cause and why
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
what dental problems does clef lip and palate cause and why
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
explain facial clefting and what dental representations would this include
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
at what age do prescriptions become free
65
197
what NICE guideline covers oral health for elderly
48
| provide oral and dental care in care homes
198
what oral changes occur with old age
loss of teeth and heavy decay
bone resorption
tooth sclerosis causing reduced sensitivity
changes to oral mucosa becoming variably less or more flexible
199
which bones grow by ECO and IMO
```
ECO = most long bones in body, mandible and cranial base
IMO = cranial vault and facial skeleton and clavicle
```
200
describe IMO
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
what are Haversian systems
unit of compact/cancellous bone
| Rings of bone (osteon) with central blood vessels and nerve supply (harversian)
202
what are the three phases of ECO
(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
what cells are involved in cartilage formation (3)
stem cells - ectomesenchymal or mesechymal
differentiate into chondroblast
mature into chondrocyte --> secrete cartilage matrix
204
what 3 zones do we find in bones growing by ECO
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
what 3 things happen during the cartilage/bone interface of EMO
apoptosis of chondrocytes
angiogenesis blood vessel formation (for Haversian systems)
ossification and mineralization of cartilage matrix = bone formation
206
compare the structure and position of osteoclasts and osteoblasts
osteoblasts: small, cuboidal, single nucleated cells found on bone surface
osteoclasts: large multinucleated cells found outside bone surface
207
what 3 situations does remodelling occur
converting woven bone into cancellous bone
make new bone
break down existing bone
208
compare bone resorption time and deposition time
```
resorption = 3-4 weeks
deposition = 3-4 months
```
209
compare bone fracture and tooth socket healing
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
does tooth socket healing occur by IMO or ECO
IMO
211
explain bone remodelling
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
what is a common IMO disorder
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
what are the dental and bodily affects of cleidocranial dysostosis
```
affects gene acting on osteoblast and chondrocyte differentiation
reduced or absent clavicle
reduced development of cranial vault
severe malloclusion
late eruption
```
214
explain a common ECO disorder
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
why do we get more cancer with age
worse cell turnover
reduced ability to fix DNA
accumulation of gene errors
216
why is cerviacle cancer more prevelent in low income areas
less education
less vaccination
less screening
217
what dietary/body factors have higher risk factors for cancer
alcohol
lack of fibre
processed red meats
body fatness
218
How common is oral cancer, which sex is more likely and what are some high risk factors
8th most common cancer
men 3x more likely
obesity, smoking, alcohol, HPV, asbestos
219
what is Ehlers-Danlos syndrome
Mutations in type V collagen, a regulator of type I collagen fibrillogenesis
poor wound healing, easy bleeding
Stretchy skin
220
what is dry socket and what 2 types of osteitis are there for dry socket
early disruption of healing extraction socket
| alveolar osteitis and fibrolytic osteitis - inflammation of alveolar socket bone
221
what is rombergs disease
Romberg’s disease produces hemifacial idiopathic atrophy where the muscles on one side of the phase occur
222
a patient has a random loss of function of half of their face and structure seems to be degrading. what are 2 differential causes
stroke
rombergs disease - hemifacial atrophy of the face
Bells Palsey
223
how can cancer move
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
what abilities do tumour cells gain
```
increased motility
alter adhesion molecules
make poor basement membrane
increase protease production or reduce inhibitors
alter ECM
```
225
how do carcinomas and sarcomas spread
Carcinomas (epithelial malignant) tend to spread through lymphatics and eventually the blood
Sarcomas (connective tissue malignant) spread through the blood
226
what are some metastatic and non-metastatic effects and malignant cancer
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
what staging system is used to grade cancer at diagnsosis and what is it based on
```
TNM histologically
Tumour Size
Node number
Metastases (absent, present)
stage 1-4
```
228
what is a common treatment of posterior tongue cancer
surgical dissection of tongue
removal of lymph nodes
splitting of jaw
229
what are some side effects of cancer treatment
```
tiredness
sickness
loss of hair
fatigue
scarring
```
230
what are some dental side effects of oral cancer treatment
```
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
what is IMRT
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
what can be used to avoid irradiation of parotid gland during oral cancer treatment
IMRT radiotherapy - intensity modulated radiotherapy
233
how do tumour cells prevent T cell action
on their surface they have an atni-PD-L1 antigen o their surface which interferes with T cell action
234
how does radiotherapy work
using very high doses of radiation to ionise and destroy cancer cells
235
how does chemotherapy work
inhibitors growth factors used by tumour cells (and other cells) in blood stream to prevent further growth of tumours
236
what are 2 syndromes that could be causes as a non-metastatic affect of a cancer in a gland
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
where is human growth hormone secreted
the pituitary gland
238
where does the pituitary gland reside
pituitary fossa close to the optic chiasm
239
what are some signs of a cancer in the pituitary gland
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
what is acromegaly and when does it occur
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
give two possible cancers that cause an increased hGH level
anterior pituitary adenoma or adenocarcinoma
| lung adenocarcinoma for some reason differentiate into pituitary cells
242
how does gigantism occur
increase in size of growth plates and activation of them before their closure + increased hGH
243
what are some oral manifestations of acromegaly (growth hormone syndrome)
occurring in adulthood:
- spacing between teeth
- unusual changes to nose
- enlarged lips
- marks on inside of cheeks
244
why must we identify acromegaly early on
it can lead to increased levels or not just bone but heart tissue
can lead to severe cardiac problems if untreated
245
what stimulates release of growth hormone
growth hormone releasing hormone
| from the hypothalamus
246
what affects does growth hormone have on the body
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
what other hormone can we study instead of GH and why
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
what is IGF-1 and why is it useful
insulin-like growth factor 1
| stimulated release by GH and helps us study GH as it is less fluctuating
249
which 2 glands does IGF-1 act on and how
inhibits production of GHRH from hypothalamus
| inhibits release of GH from pituitary gland
250
what affect does oestrogen have on growth
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
what affects does the time of puberty have on growth of girls
earlier the puberty initiation = smaller the woman
| less gradual release of oestrogen so less gradual release of growth hormone
252
what causes sexual mandibular dimorphism
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
what affect do androgens have on growth
encourage lengthening and density increase of bones
254
why does a woman have a shallower angle of mandible than a man
```
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
what are the functions of IGF-1
inhibits GH and GHRH
causes proliferation of myofibrils for muscle growth - hyperplasia
causes proliferation of chondrocytes for cartilage growth and bone growth
256
what affect does thyroid hormone have on growth
thyroid hormone stimulates release of growth hormone
effects osteoblasts and chondrocytes
drives IGF-1 for growth
257
where is the main acting site of IGF-1 on growth
epiphyseal plates
cartilage plates at ends of bones and stimulate chondrocyte proliferation
causing ECO bone lengthening (androgens also stimulate this)
258
why are obese boys taller than not obese boys
obese boys eat more sugar and release more insulin
| insulin acts on epiphyseal plates similar to insulin causing growth of ECO bones
259
what is the main effect of hypothyroidism
shorter stature
| due to less activation of GH and therefor less action of IGF-1 on epiphyseal plates
260
what causes the 2 main peaks, and when, of IGF-1
Thyroid hormone peaks pre-puberty increasing IGF-1 release
| Growth hormone is high during puberty causing increased IGF-1 release
261
what affect do glucocorticoids have on growth and long term
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
what are some side effects of glucocorticoids
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
what types of single point mutations can we get
change in amino acid = little affect
frameshift by addition/removal = large effect
introduce STOP codon leading to truncation
264
how can mutation lead to truncation
introduce a STOP codon into DNA
| leads to premature stopping of transcription
265
what types of DNA mutation are there
```
single base mutation
-no change
-frameshift
-stop codon added
Gene amplifications
Chromosome translocation
```
266
what are pro-oncogenes and where are they relevent
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
what genes are likely to cause cancer if mutated
pro-oncogenes controlling expression of genes turn to oncogenes
tumour suppressor genes that inhibit proliferation
apoptosis genes like BCL-2
Cell cycle genes
268
what is the two hit hypothesis
where the gene of one allele is damaged already/inherited
| other gene sporadically gets mutated causing no healthy gene = cancer
269
what is cephalometry and when is it used
radiographic imaging to measure planes of the skull. Can help determine treatment plan and growth
270
what is the most common cephalograph
lateral
271
at what point do we get a developed embryonic structure
3-4 weeks post conception
272
what marks the posterior border of an embryo
mesenchymal somites up to the occipital somites
273
what do we find at the top of an embryo from the lateral view
posterior - occipital somite's
embryonic head with frontonasal process
anterior pharyngeal arches
274
what do the somite develope into
vertebrae and ribs
275
what do we find between the frontonasal process and pharyngeal arches and what will it develop into
stomodeum
| mouth
276
how many pharyngeal arches do humans have
4 with 5 and 6 forming the pericardiac sac (heart)
277
what is the stomodeum and what membranes make it up
primitive mouth
between frontonasal process and pharyngeal arches
made by a very thin buccopharyngeal membrane of internal endoderm and external exoderm
278
what is the buccopharyngeal membrane and when does it break down
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
where do we find the optic placode and what is its relevance
lateral of frontonasal process
| thickened epithelium that will turn into the eyes
280
what is the growth pattern of early pharyngeal arches
proliferate bilaterally towards the midline to join up and form sutures
281
describe the structure of pharyngeal arches
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
why does it appear that the human embryo has 5 phayngeal arches
actually have 4
| highest arch 1 is split in two: maxillary and mandibular
283
which parts of the body does acromegaly affect
affects ECO epiphyseal plates after closure e.g. mid-age
| e.g. mandible, nose and hands carry on growing
284
what is the innervation of the 4 pharyngeal arches
```
I = trigeminal (senosry) CNV
II = Facial (motor) CNVII
III = glossopharyngeal (tongue) CN IX
IV = Vagus (neck) CNX
```
285
what genes control different proliferations in different pharyngeal arches
HOX genes found in rhombomeres
286
explain the pathway of recurrent laryngeal nerves and why
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
what muscles do the pharyngeal arches innervate
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
what cartilages come from which pharyngeal arches
I: meckels cartilage - teeth, incus, malleus
II: Stapes, Styloid process and ligament and Greater cornu of hyoid
III: majority of hyoid
IV: thyroid
289
how does the ear form embryologically
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
what forms from the pharyngeal pouches - endoderm
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
how do we know the maxillary and mandibular pharyngeal arch are part of the same phayrngela arch
both innervated by the same nerve: CNV therefor due to HOX genes, same arch
292
when does the first pharyngeal arch separate into Mn and Mx
4 weeks post conception
293
what are the two reaons why it is important that the buccophayrngeal membrane breaks
to allow entrance ito the primitive gut
| to separate nose and mouth
294
how and when does the nose and primary palate start to form
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
what do nasal placode cells eventually turn into
oldfactory epithelium
296
how does the primary palate form
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
describe the growth of the maxillary process of the first pharyngeal arch
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
what two processes grow from the maxillary process and how do they grow
```
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
what factor is released, and by what, for growth of the palate and what would a deficency in this lead to
FGF10
excreted by the ectomesenchyme
cleft palate
300
what happens to the embryonic head at 8 weeks (explain why palatal elevation occurs(3))
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
at what stage do the palatal processes meet
10 weeks post conception
302
what fusion occurs at week 10 of embryonic stage (3)
palatine processes fuse:
together
with primary palate
with nasal septum
303
what controls, and how does, fusion of maxillary processes at week 10
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
when should palatine fusion have occured
week 12
305
what factors and proteins are released during fusion of palatine processes
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
what derives the different part of the palate and at how many week post conception do they occur
```
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
what is the evolutionary advantage of the palate
allows us to breathe and masticate at the same time
308
what forms the borders of the mouth during embryological growth
fusion of the maxillary and mandibular processes
309
during week 12-15 what can we see occurring in the palate (2)
anterior 2/3 invaded by bone
| posterior 1/3 invaded by muscles of arch 4 (CNX)
310
what causes cysts at the midline palate
fusion of palatal processes and nasal spine can leave remnant of epithelium
can eventually form epithelium bound cysts
311
what causes the protrusion of the nose (2)
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
what is macrostomia
larger macro, mouth stomia
| wider mouth caused by failure of fusion of the maxillary and mandibular processes of pharyngeal arch 1
313
what pregnancy factors can lead to clefts
alcohol
smoking
folic acid deficiency
314
what causes a unilateral cleft lip and palate
failure of fusion between one side of the maxillary palatine process and the primary palate
315
what causes a midline cleft palate
failure of the fusion between the 2 maxillary palatine processes
316
what can cause cleft palate to occur
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
what mutaitons might lead to cleft lip and palate
transcription factor Msx-1 release by ectoderm
| apoptotic factor BMP2 and BMP4 released by ectomesenchyme
318
what forms the upper lip
merging of the medial walls of the nasal cavity and palatine processes of pharyngeal arch 1
319
what causes cleft lip
fusion of the medial walls of the nasal cavity and the maxillary palatine process
320
differentiate cleft lip from clef palate
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
what is it called when our population is ageing and getting more disease
demographic shift
322
what are some accelerated growth disorders
Wreners Syndrome
| Hutchinsons Disease
323
what are the social and medical models for disability
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
compare impairments and disabilities
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
what is a handicap
a disadvantage in life to the pt due to an impairment or disability that limits fulfilment of a role
326
why is the medical model of disability flawed and what should replace this and why
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
how do dental practices bring in handicaps
wheelchair users cannot sit in the chair or get up stairs
328
why might dentine sensitivity be classed as a disability
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
histologically, what is found lateral to the Meckel's cartilage in normal embryonic development
condensing ectomesenchymal cells into the mandible bone
330
what is woven bone
immature bone with disordered matrix (high collagen III)
331
what is the shape and function of osteocytes
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
what proteins are rich at reversal lines
Sialoprotein and Osteopontin
333
how can we identify reversal lines and what are they
dark blue lines
representing bone remodelling - changing from osteoclastic to osteoblastic activity
high in sialoprotein and osteopontin
334
when do we get bone remodelling of alveolar bone (3)
exfoliation of teeth and changing alveolar socket
Orthodontic treatment artificially causing bone remodelling
when the tooth is lost and alveolar bone resorbs
335
what would we see on a Pagets Disease pt histological bone
lots and lots of reversal lines
336
what are the 5 zones of a ECO transition
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
what is the spheno-occipital sychondroses and why is it special/important. Which disease affects this
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
which bone do we find the magnum foramen in
occipital bone of cranial base
339
what age does palatal elevation occur
8 weeks
340
what age does palatal elevation occur
8 weeks
341
how long can separation anxiety affect a child
from 18 months to 5 years
342
at what age can a baby start to understand simple words and turn toward sound
6 months
343
what happens to a baby at age 6 months
```
can sit by them self
curious and puts things in mouth
crys when left by parent
turns toward sound
understands simple words
```
344
at what age can a baby start to wlak
12-18months
345
what happens at 12-18months
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
at what age can a baby recognise themselves in a picture
2 years
347
what happens at 24 months old
walk up and down stairs
recognise themself in pcitures
understand 200 words
easily frustrated
348
what changes occur from 2years old to 5 years old
```
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
what is a schema
unit of knowledge
| used to measure a persons understanding of the world
350
compare assimilation and accommodation of knowledge
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
what are the 4 phases of Piagets theory of development
Sensorimotor 0-2
pre-operational 2-7
concrete operational 7-12
formal operational >12
352
explain the first phase of Piagets theory of devlopments
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
explain the second phase of Piagets theory of cognitive development
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
explain the 3rd phase of Piagets theory of cognitive development
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
explain the 4th phase of Piagets theory of cognitive development
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
why is there little point in telling a child health benefits of toothbrushing until the age of 12
age of 12 the child enters the fourth stage of Paigets theory of cognitive development: functional operational
able to grasp future concepts
357
what are some faults with paigets theory of cognitive development
children progress at different rates
doesn't account for disabilities
doesn't account for different cultural upbringings
358
Explain functional operational Ego-Centralism and how it affects life
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
what is the term for a young person around the age of 12 that feels very unconfident, uncomfortable and awkward
functional operational ego-centrisism
360
what is a developmental disorder
a disorder which affects 1 or more developmental domain
| pt is outside of 2 SD of the mean
361
what causes developmental disorders
```
Postnatal infections like meningitis
Maternal smoking, alcohol and drugs
Genetic Factors
Malnutrition
Social factors like income, lone parenting etc
```
362
how do we adapt our actions around a toddler
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
how do we adapt our actions with a 3-4 year old
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
how do we adapt our actions when working school age children
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
how do we change our actions with a teenage patient
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
what is an autism spectrum disorder
neurodevelopmental disorder with unknown aetiology
affects 1:100 children
4x more likely in males
accompanies with ADHD/Seizures and 50% with learning difficulties
367
how do we adapt our actions with a autistic patient
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
when does growth occur at its fastest rate and how fast?
2nd trimester of pregnancy
| 2cm a week
369
how do we find BMI
mass divided by height squared
370
what determines growth in infancy, childhood and teenage years
```
infancy = nutrition
childhood = GH
teenage = sex hormones and GH
```
371
give some determinants of growth
```
nutritional deficency
malabsorption = coaeliac
systemic disease = hypothyroid, hypopituitary, heart problems
steroid excess
inherited = achondroplasia
```
372
what can birth defects be divided into
single/isolated defects affecting only 1 system
| multiple defects
373
what can multiple defects of birth defects be further divided into
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
what causes dons syndrome
trisomy 21
| third copy of 21st chromasome
375
what are some dental manifestations of Trisomy 21
```
downsyndrome
Large, fissured tongue
Periodontal disease
Hypodontia
Microdontia
Enamel defects
Class 3 malocclusion due to maxillary retrognathia
```
376
what causes dentinogenetic imperfecta
DSPP dentine sialophosphoprotein mutaiton that usually coats non-collagenous dentine proteins
affects the non-collagenous proteins of dentine
377
how many people are affected by dentinogenesis imperfecta
1 in 6000-8000
378
what are some sings and symptoms of dentinogenetic imperfecta
```
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
what are some signs of osteogenesis imperfecta
```
bone fragility (vertebral)
Connective tissue disease with thin blood vessels (bruise easily)
Poor muscle
Blue sclera
Progressive hearing loss
```
380
what causes osteogenesis imperfecta
inherited autosomal mutation of a collagen gene effecting the production/processing of collagen 1
381
what are two possible causes of rickets
malnutrition - not taking in enough vitamin D inhibiting calcium/phosphate uptake
X-linked hypophosphotatemia - dominant X linked disruption in calcium/phosphate metabolism
382
what are some oral manifestations of rickets (3)
Large pulp chambers
elongated pulp horns
Abscesses in the absence of caries
383
there are abscesses in the absence of caries. what growth disorder can cause this
X-linked hypophsophatemia (rickets)
384
which gene is affected by X-linked hypophosphatemia
FGF23 involved in metabolsim of phosphate and calcium
385
what oral manifestations of cleidocranial dysplasia are there
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
why is there a mis-alignment of maxilla and mandible in cleidocranial dysplasia
affects IMO
mandible grows partially due to ECO however maxilla grows solely by IMO
Causes class III and wider mandible than maxilla
387
what is the enamel organ
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
where does the IDE and EDE meet
cerviacle loop
389
how does space for PDL to insert onto the cementum form
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
what does the dental follicle differentiate into
cementoblasts
| fibroblasts
391
what is mantel dentine and why is it formed
pre-odontoblasts secrete dentine matrix before they are fully devloped
this dentine has higher ECM than collagen
392
how mineralized is cementum
55%
393
what is the order of eruption of primary teeth
ABDCE
394
when does the crown of primary teeth start mineralizing
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
when are primary crowns fully mineralized
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
when do primary crowns erupt
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
when is the root fully developed of primary teeth
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
what is the order of eruption of the secondary teeth
```
6
1
2
4
5
3
7
8
```
399
how do we find the age of a tooths crown start, crown finish, crown erupt, root finish
```
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
when does the secondary canine start devloping
age 2
401
how long does the canines root take to form
6 years
402
when does the crown start forming of wisdom teeth
12 years old
403
which is the only tooth to erupt with a fully formed root
secondary canine
404
when do mandibular erupt in relation to maxillary teeth
mandibular erupt 6 months before maxillary
405
if the LL6 erupts at 6 years old, when should the LR6 and UR6 erupt
within 6 months
406
what are the first secondary teeth to erupt
mandibular first molars
407
what happens at 4 weeks post conception
buccopharyngeal membrane breaks down to stomodeum
| first arch split into maxillary and mandibular process
408
what happens at 5 weeks post conception
invagination of nasal placode
| growth of nasal processes
409
what happens at 6 weeks post conception
outgrowth of palatal processes and tectoseptal processes
primary palate formed
md fusion at midline
410
what happens at 8 weeks post conception
tongue drops
| palatine elevation
411
what happens at 10 weeks post conception
fusion of palatine, primary palate and medial nasal processes starts
412
what happens at 12 weeks post conception
fusion of processes ends
413
what happens at 12-15 weeks post conception
differentiation of cells of the oral cavity
414
what do we need for a dental ageing evaluation
OPT radiograph
415
what are the disadvantages and advantages of dental ageing
```
+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
how are teeth rated whilst doing dental ageing
A to H
| A being not developed H being fully developed
417
what is chronological age
years from birth
418
what is biological age
based on transitional change in biological landmarks
419
why do we do dental ageing
dental ageing corresponds strongly with chronilogical age
useful for forensics
estimating ages of children with no parents
420
what is the hayflick limit
number of times a cell can divide before being senescent - telomeres
421
is telomeres length/hayflick limit evolutionary or programmed ageing
evolutionary
422
what type of disease is crouzons
craniosystenosis
| mishapen head due to premature fusion of sutures causing brain to expand against formed skull
