29. Ageing Flashcards
1
Q
What is ageing?
A
- a progressive decline in ability to respond effectively to stress of environment
- a person usually over 65
- by 2025, over 2 million people will be over 80
2
Q
Speed of aging depends on … and …
A
- genetics
- lifestyle
3
Q
Age changes happen to what dental tissues?
A
- enamel
- dentine
- pulp
- cementum
- PDL
- alveolar bone
- oral mucosa
- salivary glands
4
Q
Age changes in enamel
A
- plaque develops on surface
- colour
- thickness
- mineral content
5
Q
How does discolouring of teeth occur with age?
A
- progressive thinning of enamel due to tooth wear and thickening of yellowish dentine
- this shines through semi-translucent enamel contributing to darkening
- stains (coffee, wine, tea) become trapped in micropscopic pits of enamel during remineralisation
- tooth whitening/bleaching only temp helps
6
Q
Darkening of enamel surface pronounces what?
A
striae of Retzius
7
Q
Influence of oral environment on age changes in enamel
A
- composition of saliva, fluoride, microorganisms
- over time, surface of enamel becomes more mineralised by incorporation of fluoride present in saliva (HA to FA)
- fluorapatite is harder than hyddroxyapatite - older people are less susceptible to caries
- bonding of dental materials to enamel does not appear to be affected with age
8
Q
Repair of enamel by remineralisation
A
- enamel cannot regenerate because ameloblasts are lost at the end of development
- enamel (physico-chemical) repair process is remineralisation by re-incorporation of calcium, phosphate and fluoride ions that are present in saliva
- imbalance in de-re-mineralisation cycle - shift towards demineralisation causes caries (white stop lesion is early sign)
9
Q
How do early stage caries show?
A
- active, non-cavitated chalk white lesion
- superficial defect
10
Q
Dynamic appearance of white spot lesions
A
- surface zone (intact enamel, remineralisation caused by ion precipitation from saliva)
- body of lesion (enamel destruction)
- dark zone (enamel remineralisation)
- translucent zone (enamel demineralisation)
- reversible if surface enamel remains intact and acid producing bacteria are removed
11
Q
Age changes in dentine
A
- secondary dentine
- intratubular dentine
- sclerotic dentine
- tertiary dentine
- dead tracts
12
Q
How does secondary dentine happen in age?
A
- normal continuation of dentine formation by existing odontoblasts lining pulp space after completion of tooth roots
- slower formation than primary around 0.5 vs 4 microm a day
- irregular distribution - more common on roof and floor of pulp chamber
13
Q
Explain how secondary dentine forms contour line of Owen
A
- tubules are continuous with primary dentine tubules but fewer in number
- tubules can bend creating contour line of Owen between primary and secondary dentine
14
Q
How does secondary dentine affect pulp chamber?
A
- reduces size of pulp chamber and root canals (pulp recession)
- pulp chamber can be completely occluded and root canals are very narrow
- endodontic treatment can be challenging for older patients
- cavity prep in younger carries risk of exposing pulp
15
Q
How does peritubular/intratubular dentine come with age?
A
- forms on walls of dentinal tubules
- begins to form in outermost dentine
- forms by precipitation of calcium phosphate ions from dentinal fluid
- about 90% mineralised
- usually no collagen
- can fill whole dentinal tubule - completely occlude dentine tubules (sclerotic dentine)
16
Q
What is sclerotic dentine? How does it form?
A
- complete occlusion of dentine tubules by peritubular dentine
- dentine becomes transparent
- physiological factor is ageing - found mostly in roots
- pathological factor - response to caries found in carious lesion and pulp
17
Q
2 types of tertiary dentine
A
- reactionary
- reparative
18
Q
How does reactionary dentine form?
A
- slower response from existing odontoblasts lining dental pulp
- few tubules
- response to tooth wear/attrition
19
Q
How does reparative dentine form?
A
- rapid response
- new odontoblast-like cells induced from dental pulp stem cells
- less structure
- response to caries/cavity prep
20
Q
How does dentine respond to tooth wear?
A
- slow, natural wear of crown stimulates peritubular dentine formation
- dentine becomes less permeable and insensitive if exposed
- important adaptation if enamel is worn away
- to compensate for dental tissue loss, reactionary dentine forms slowly in pulp
21
Q
A primary incisor with little tooth wear would have a defined pulp horn and large pulp volume. A worn cusp would have …
A
- pulp horn filled with reactionary dentine
- smaller pulp volume
22
Q
Explain dead tracts
A
- group of odontoblasts die due to continuous, strong stimulus (attrition or caries)
- results in reparative dentine formation - acts to seal off pulp from invading microorganisms
- empty dentinal tubules contain air causing dark appearance on ground section of teeth (dead tracts)
23
Q
List age changes in dental pulp
A
- decreased number of cells
- less nerve and blood vessels
- more fibrous
- size reduction of pulp chamber
- calcified structures in pulp more common in older people (true pulp stones/denticles, false pulp stones, diffuse calcifications)
24
Q
Compare true and false pulp stones and diffuse calcifications
A
- true are made of organic matrix and dentine tubules
- false are concentric layers of calcified degenerated pulp tissue
- diffuse are not pulp stones - associated with blood vessels or collagen fibres along the long axis of radicular pulp
25
Q
Age changes in cementum
A
- thickness increases 3 times from 16-70
- not known if increase is linear, forms at root apex in response to attrition at occlusal surface
- mainly cellular cementum
- hypercementosis - extreme increase in cementum
26
Q
Define ‘hypercementosis’
A
increase in cementum
27
Q
Age changes in PDL
A
- mainly based on animals
- decrease in cell numbers, density and mitotic activity
- fibroblasts have shorter live spans, diminished collagen synthesis and degradative activity
- increased collagen fibrosis, thicker fibre bundles and mineralisation of fibres
- irregular insertion of Sharpey’s fibres
- teeth become less ‘mobile’ - decrease remodelling capacity
- incidence of periodontitis is higher with age
28
Q
Changes in alveolar bone with age
A
- loss of teeth so loss of alveolar bone
29
Q
Changes in oral mucosa in age
A
- thinning of tongue epithelium on dorsal and lateral surfaces
- reduced taste sensation
- gingival recession - but could be due to poor oral hygeine
- increasing susceptibility to precancerous lesions and oral cancer
30
Q
Age changes in salivary glands
A
- decrease in amount of glandular tissue
- increase in fibrous tissue, fat cells and inflammatory cells
- dry mouth/xerostomia - usually not present in healthy older people, associated with increased use of medications, increases rate of attrition (due to reduced enamel mineralisation)
31
Q
What is physiological attrition?
A
- tooth wear caused by mastication
- e.g contact with food particles
32
Q
What is pathological attrition?
A
tooth wear caused by chewing with abnormal movement or habitual jaw clenching
- e.g bruxism
33
Q
What is abrasion?
A
- tooth wear caused by frictional contact with foreign objects
- e.g pip smoking
34
Q
A
35
Q
What is erosion?
A
- progressive loss of hard tissues due to chemical dissolution
- e.g acidic drinks
36
Q
What surfaces are affected by physiological attrition?
A
- interproximal and occlusion surfaces
- more in men as larger masticatory force
37
Q
What is bruxism?
A
- habitual jaw clenching and tooth grinding
- flat occlusal plane
- dentine hypersensitivity due to exposed dentine
38
Q
What is V-shaped cervical lesion?
A
- lesions caused by excessive tooth brushing and abrasive toothpastes
39
Q
What is incisal wear/grooves?
A
- due to habits like pipe smoking or nail biting
40
Q
Define ‘erosion’
A
- chemical dissolution of hard tissues
- e.g non-bacterial acids
41
Q
Erosion sources
A
- intrinsic (from stomach acid)
- extrinsic such as …
- dietary - carb drinks, fruit juicecetc
- environmental - competitive swimmers, wine tasters
- medication - iron tonics, vitamin C supplements
42
Q
How can erosion be caused by stomach acid?
A
- regurgitated stomach acid - acid reflux/repeated vomiting or eating disorders like anorexia, bulimia
- after vomiting, tooth brushing should be avoided for an hour
- chewing gum increases saliva production and buffering
43
Q
Chemical basis for erosion
A
- enamel doesn’t dissolve in calcium-phosphate super-saturated saliva (pH7) but at pH less than 6, saliva is under-saturated
- acidic dissolution initiates erosion and makes tooth susceptible to abrasion
- the lower the pH of oral env, the higher is enamel surface loss
- saliva is critical for dilution, buffering, removal of acid
44
Q
Factors contributing to dietary erosion
A
- amount of drink consumed
- frequency and manner of consumption
- timing of consumption
- stength of acid
45
Q
Groups at greater risk of erosion
A
- diabetics who consume fruit juice
- people with lower salivary flow (older on meds) should avoid acidic drinks
- children with asthma (inhaling lowers pH)
- consumers of sports drink (high sugar)
- ecstasy and cocaine users (xerostomia, bruxism, irritation of gingiva caused)
