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Resto > No bacterial dental pathology > Flashcards

No bacterial dental pathology Flashcards

1
Q

Etiology:

Multifactorial

A
  1. Diet
  2. Parafunction
  3. Functional demand
  4. Detective enamel and dentin
  5. Habits
  6. Recession
  7. Medication
  8. Saliva flow
  9. Abrasive dentifrices and hard brushing
  10. Abrasive restorative materials (unglazed porcelain)
  11. Stress
  12. Genetic
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2
Q

What include diet?

A

exposure to erosive foods

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3
Q

What include parafunction?

A

bruxism

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4
Q

What include functional demand?

A

loss of teeth

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5
Q

What include defective enamel and dentin`

A

hypoplasia

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6
Q

Whats amelogenesis imperfecta?

A

genetic disorder of tooth development affecting the enamel

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7
Q

Whats dentinogenesis imperfecta?

A

is a genetic disorder of tooth development

Affecting enamel and dentin, rapid wear, breakage

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8
Q

Fracture

A

loss of dental hard tissue due to a trauma

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9
Q

Pathological attrition:

etiology

A
  1. jau prognatisms- class III, II div 2
  2. saliva: xerostomy
  3. Alteration in teeth calcification (amelogenesis, dentinogenesis imperfecta)
  4. Hyper function. clenching and bruxism
  5. Occlusion: loss of teeth/ contacts > demand on the remaining teeth
  6. Diet: abrasive meals
  7. Habits
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10
Q

Attrition clinically:

A
  1. facets (occlusal and incisal)
  2. flat, large, smooth, shiny and polish surfaces
  3. loss of anatomical details
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11
Q

How do we distinguish a severe attrition?

A
  1. dentin exposure
  2. dentin hypertensivity
  3. Pulp exposure
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12
Q

What colour do we get in clinically attrition?

A

Scelerotic and secondary dentin: brown area

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13
Q

What can we see in X-rays by attrition?

A
  1. less pulp chamber
  2. more periodontal space
  3. Hypercementosis
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14
Q

Abrasion

A

Pathological wear of dental hard tissue through abnormal mechanical processes
(foreign objects, substances (not caused by food or contact between teeth)

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15
Q

Where do we find abrasion?

A
  1. Occlusal

2. incisal and cervical

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16
Q

Abrasion clinically:

A
  1. hard smooth surface
  2. yellow brown surfaces- if sclerosis or 3ry dentin
  3. Asymtomatic or dentin hyperthermia (hypertensivity)
  4. Cervical: wedge shaped, sharp and well defined (dentin and cementum are less wear resistant)
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17
Q

How do I know if its abrfaction or attraction?

A

check occlusion

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18
Q

Erosion

A

Pathologic, chronic, localised, painless loss of dental hard tissue cause by intrinsic or extrinsic chemical agents without bacterial involvement

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19
Q

Erosion Etiology:

A
  1. multifactorial
  2. influence of patient habits and lifestyle
  3. Due to extrinsic and instrinsic agents
  4. Biological factors
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20
Q

Erosion: Biological consequences

A
  1. change in physical properties and dental structure
  2. enamel: microhardness reduction = enamel erosion
  3. dentin: reactive dentin + pulp tubules obliteration
  4. if advanced: hypersensitivity, pulp inflammation and even necrosis and periodontal disease
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21
Q

Erosion clinically:

Advanced signs

A

Advanced signs:

  1. flat/ blurred grooves and pits
  2. Dentin exposure
  3. High restoration around worn dentin
  4. Well- defined concavities in dentin at the occlusal and incisal surfaces, specially the cusps
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22
Q

Erosion clinically

A
  • buccal an palatal surfaces of maxillary anterior teeth
  • occlusal and palatal surfaces of maxillary posterior teeth
  • buccal and occlusal surfaces of mandibular posterior teeth
  • shallow spoon shaped depression in cervical portion of the crown (maxillary anteriors)
  • loss of occlusal surface (posterior)
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23
Q

Perimolysis

A

Erosion of tooth enamel and dentin frequently associated with conditions involving chronic regurgitation of acid gastric contents (such aus bulimia or anorexia nervosa( which affects the palatal surfaces of the maxillary anterior teeth (particularly the central and lateral incisors( and the occlusal surfaces of the posterior teeth
- Acid leaves a pattern consistent with the heads position while vomiting

24
Q

Why does medication affect the pathology?

A

Cause it reduced the saliva flow, people get more stressed, they girnd more

25
Q

What factors lead to an irreversible loss of tooth structure (caries)?

A
  1. Non-hereditary/ Hypocalcification/ Hypoplasia of Enamel/Dentin
  2. Genetic disorders: Amelogenesis imperfecta. Dentinogenesis imperfecta.
  3. Fractures.
  4. Attrition (masticatory action).
  5. Abrasion (mechanical wear).
  6. Erosion (acid chemical wear).
  7. Abfraction (repeated cyclic flexion of teeth).
26
Q

Amelogenesis imperfecta.

A

Genetic disorder of tooth development affecting the enamel.

happens while the tooth is forming

27
Q

Dentinogenesis imperfecta (DI)

A

is a genetic disorder of tooth development. Affecting enamel and dentin. Rapid wear, breakage.
(same but affects both)

28
Q

Whats the loss of dental hard tissue due to a trauma?

A

Fractures

tooth is broken

29
Q

Attrition

A
  • Physiological wear of dental hard tissue as a result of
    tooth to tooth contact (friction).
  • Incisal and occlusal surfaces. Slow and progressive.
  • Physiological wear
    = 65μm/ year

If > 65μm/ year: pathological attrition Bruxism: main cause (x 3-4).

30
Q

Attrition Etiology:

A

Etiology:
‣ Age: age > dental wear.
‣ Sex: men > women
‣ Time: teeth contact aprox. 17,5 minutes/day

(the older we are, the more we present)

31
Q

Pathological attrition, Etiology:

A

‣ Jaw prognathism: Class III.
‣ Class II div 2.
‣ Saliva: xerostomy.
‣ Alteration in teeth calcification (amelogenesis, dentinogenesis imperfecta).

32
Q

Whats hyper function?

A

Clenching and bruxism

33
Q

Attrition occlusion:

A

loss of teeth/contacts > demand on the

remaining teeth.

34
Q

Attrition: Diet

A

Abrasive meals

Habits

35
Q

Attrition Prevalence:

A
  • Incisal + occlusal surface
  • Palatal surface of anterior maxillary teeth
  • Labial surface of anterior mandibular teeth
36
Q

Attrition Clinically:

A
  • Facets (occlusal and incisal).
  • Flat, large, smooth, shiny and polish surfaces.
  • Loss of anatomical details.
37
Q

Attrition clinically:

A

Severe attrition:

  • Dentin exposure.
  • Dentin hypersensitivity.
  • Pulp exposure.
38
Q

Attrition Sclerotic and secondary dentin

A

brown areas

39
Q

Attrition: xray

A
  • less pulp chamber
  • more periodontal space
  • Hypercementosis
40
Q

Attrition: Treatment

A

Prevention: Normal (physiological) attrition requieres no treatment

  • restorations
  • prosthodontics rehabilitation
  • Occlusal adjustment and mouth guard therapy if malocclusion or bruxism
41
Q

Abrasion

A
  • Pathological wear of dental hard tissue through abnormal mechanical processes. Involving foreign objets or substances repeatedly introduced in the mouth and contacting the teeth (not caused by food or contact between teeth)
  • Occlusal (similar lesion as attrition), incisal and cervical.
42
Q

Abrasion Etiology:

A
  • patients factors
  • brushing techniques
  • habits (nails biting, holding objects between. teeth)
  • materials (toothbrush, dentifrice, piercings, foreign objects, prosthodontics retainers)
43
Q

Abrasion prevalence:

A
  • cervical buccal area of anterior teeth
  • cervical buccal area of posterior teeth
  • incisal edge
  • occlusal
44
Q

Abrasion: treatment

A
  • habit correction
  • dentin desensitisation (Floride varnish etc)
  • restorative (resin, composite restoration
45
Q

Abfraction

A

Micro-structural loss of tooth substance in areas of stress concentration.

46
Q

Abfraction: Etiology

A
  • Repeated compression and flexure of the teeth
    under occlusal loading.
  • Caused by premature contact of teeth.
  • High incidence in bruxists
47
Q

Abfraction: clinically

A

•Lesions can be found only in one tooth in one
segment.
•Predominately it affects buccal surfaces of molars and premolars.
•Wedge-shaped defects limited to cervical region of the teeth

48
Q

Abfraction: enamel

A
  • Micro-fractures (hair line cracks) in cervical regions.
  • Striations, irregular horizontal bands due molecular fractures or “lines of Luder”.
  • Horizontal semilunar/dish-shaped bands. -Cusps tip invagination.
49
Q

Abfraction dentin:

A

Dentin is more elastic and able to withstand greater
tensile stress than enamel:

  • Gingival
  • McCoy notch- interproximal, circunferencial -Subgingival, lingual, multiple, alternating, angular…
50
Q

Abfraction treatment:

A
  • Occlusal adjustment
  • Restorative
  • Mouth guard

(number of teeth that are affected, any brushing techniques, habits etc.(

51
Q

Erosion Etiology- Extrinsic agents

A
  • Acidic contaminants from the working environment (industrial acids, chlorine in swimming pools, painters, wine-tasters…).
  • Medicins:
    ➡ Vit C.
    ➡ Ferric complements.
    ➡ Hydrochloric acid tablets.

Dietary acids:
➡ Implicated foods:
Fizzy drinks (pH 2.2-3.8) Fruit juices (pH 3.0-4.0) Wines (pH 3.2-4.8)
Cider and Beer (pH 3.5-4.0)

52
Q

Erosion intrinsic agents:

A

-Gastric acid
➡ Recurrent vomiting
➡ Regurgitation
➡ Reflux

Self induced eating disorders : anorexia/bulimia Somatic origin: pregnancy, GI disorders (ulcers, hernia..)

53
Q

Erosion biological factors:

A
  • Saliva: dilution and elimination of erosive agent. Acid neutralization and buffering capacity: demineralization.
  • Tooth structure: tooth composition and formation.
  • Anatomy and occlusion: attrition. Para-functional disease could be accelerated by erosion.
  • Acid-wear: tooth > susceptible to attrition and abrasion.
54
Q

Erosion clinically first sign:

A
  • Loss of enamel shine.
  • No bacterial plaque (macroscopic).
  • Round and polished surfaces. Loss of micro- anatomy.
55
Q

Erosion: Treatment

A
  • Eliminate or control etiological factors.

- Restorative.

56
Q

Conclusions

A
  • The causes of tooth surface loss can be multifactorial and hence difficult to eliminate.
  • Tooth wear can be classified as physiological or pathological but no universal guidelines are available to differentiate them. The same tooth wear may be considered as physiological for the elderly, but pathological for a young person.
  • Loss of tooth substance (tooth wear) could alter aesthetics and function.
  • A systematic treatment approach should be needed to manage the situation.

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