29. Ageing Flashcards

(45 cards)

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
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2
Q

Speed of aging depends on … and …

A
  • genetics
  • lifestyle
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3
Q

Age changes happen to what dental tissues?

A
  • enamel
  • dentine
  • pulp
  • cementum
  • PDL
  • alveolar bone
  • oral mucosa
  • salivary glands
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4
Q

Age changes in enamel

A
  • plaque develops on surface
  • colour
  • thickness
  • mineral content
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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
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6
Q

Darkening of enamel surface pronounces what?

A

striae of Retzius

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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
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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)
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9
Q

How do early stage caries show?

A
  • active, non-cavitated chalk white lesion
  • superficial defect
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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
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11
Q

Age changes in dentine

A
  • secondary dentine
  • intratubular dentine
  • sclerotic dentine
  • tertiary dentine
  • dead tracts
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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
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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
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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
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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)
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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
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17
Q

2 types of tertiary dentine

A
  • reactionary
  • reparative
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18
Q

How does reactionary dentine form?

A
  • slower response from existing odontoblasts lining dental pulp
  • few tubules
  • response to tooth wear/attrition
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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
Age changes in cementum
- 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
Define 'hypercementosis'
increase in cementum
27
Age changes in PDL
- 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
Changes in alveolar bone with age
- loss of teeth so loss of alveolar bone
29
Changes in oral mucosa in age
- 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
Age changes in salivary glands
- 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
What is physiological attrition?
- tooth wear caused by mastication - e.g contact with food particles
32
What is pathological attrition?
tooth wear caused by chewing with abnormal movement or habitual jaw clenching - e.g bruxism
33
What is abrasion?
- tooth wear caused by frictional contact with foreign objects - e.g pip smoking
34
35
What is erosion?
- progressive loss of hard tissues due to chemical dissolution - e.g acidic drinks
36
What surfaces are affected by physiological attrition?
- interproximal and occlusion surfaces - more in men as larger masticatory force
37
What is bruxism?
- habitual jaw clenching and tooth grinding - flat occlusal plane - dentine hypersensitivity due to exposed dentine
38
What is V-shaped cervical lesion?
- lesions caused by excessive tooth brushing and abrasive toothpastes
39
What is incisal wear/grooves?
- due to habits like pipe smoking or nail biting
40
Define 'erosion'
- chemical dissolution of hard tissues - e.g non-bacterial acids
41
Erosion sources
- intrinsic (from stomach acid) - extrinsic such as ... - dietary - carb drinks, fruit juicecetc - environmental - competitive swimmers, wine tasters - medication - iron tonics, vitamin C supplements
42
How can erosion be caused by stomach acid?
- 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
Chemical basis for erosion
- 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
Factors contributing to dietary erosion
- amount of drink consumed - frequency and manner of consumption - timing of consumption - stength of acid
45
Groups at greater risk of erosion
- 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)