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Craniofacial and Tooth Biology > 29. Ageing > Flashcards

29. Ageing Flashcards

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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
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)

Craniofacial and Tooth Biology (25 decks)

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