Day 2 lecture 2 Flashcards

1
Q

Didja read?

A

40 out of slides, 3 or 4 from tying slides together, 5 out of book.

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2
Q

Caries

A

Demineralization of tooth structure, breakdown of protein structure.

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3
Q

Modified Keyes-Jordan diagram.

A

See slide image - 60+ bacteria, maybe as many as 300 play a role. Good bacteria can also make them behave badly. Poverty level is a huge determinant, until middle age. After middle age, wealthy more likely to get decay than the poor (secondary, not a cause or prevention, just an indication).

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4
Q

Age factor

A

Physical changes in body - old people take drugs - number one side effect is drymouth.

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5
Q

Possible caries

A

Some areas of noncavitated caries have superficial stain

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6
Q

caries activity

A

characterized by localized demineralization and loss of tooth structure. Cariogenic bacteria in the biofilm metabolize refined carbohydrates for energy and produce organic acid by-products. These organic acids, if present in the biofilm ecosystem for extended periods, can lower the pH in the biofilm to below a critical level (5.5 for enamel, 6.2 for dentin). The low pH drives calcium and phosphate from the tooth to the biofilm in an attempt to reach equilibrium, hence resulting in a net loss of minerals by the tooth, or demineralization. When the pH in the biofilm returns to neutral and the concentration of soluble calcium and phosphate is supersaturated relative to that in the tooth, mineral can then be added back to partially demineralized enamel, in a process called remineralization. (pg. 41, Sturdivant)

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7
Q

pH enamel

A

5.5

hydroxyapatite

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8
Q

pH dentin

A

6.2

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9
Q

Ecological plaque hypothesis

A

Fermentable sugar (forms acid) lowers pH, makes more MS and lactobacilli, more demineralization. 58 of other bacteria also increased. Not exactly true, since at low enough pH the “good bacteria” will go bad.

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10
Q

pH enamel hydroxyfluorapatite

A

4.5 for hydroxyfluorapitite

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11
Q

ph 8

A

calcium fouride CaF2, phosphates, like hydroxyapatite

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12
Q

pH 6

A

hydroxyapatite demineralizes

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13
Q

pH 4

A

hydroxyfluorapatite demineralizes

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14
Q

Symptoms

A

Demineralization lesions in teeth

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15
Q

Treatment, symptomatic

A

restoration of cvitated lesions

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16
Q

Treatment, therapeutic

A

Improvement of host resistance by - biofilm control - elevating biofilm pH - enhancing remineralization.

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17
Q

Post-treatment

A

Re-evaluate risk factors, find how to negate risk factors.

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18
Q

Dental plaque

A

is a term historically used to describe the soft, tenacious film accumulating on the surface of teeth. Dental plaque has been more recently referred to as a plaque biofilm, or simply biofilm, which is a more complete and accurate description of its composition (bio) and structure (film)

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19
Q

Biofilm

A

is composed mostly of bacteria, their by- products, extracellular matrix, and water

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20
Q

Bacterial plaque formation

A

After teeth cleaning, within 30min to 1 hour acquired pellicle forms with salivary proteins and cells. Protects (antibodies), reduces friction. Both acidic and basic proteins that
adsorb calcium and phosphate ions

21
Q

▪Caries lesion.

A

Tooth demineralization as a result of the caries process. Other texts may use the term carious lesion. Laypeople may use the term cavity.

22
Q

▪Smooth-surface caries.

A

A caries lesion on a smooth tooth surface.

23
Q

▪Pit-and-fissure caries.

A

A caries lesion on a pit-and-fissure area.

24
Q

▪Occlusal caries

A

A caries lesion on an occlusal surface.

25
Q

▪Proximal caries

A

A caries lesion on a proximal surface.

26
Q

▪Enamel caries

A

A caries lesion in enamel, typically indicating that the lesion has not penetrated into dentin. (Note that many lesions detected clinically as enamel caries may very well have extended into dentin histologically.)

27
Q

▪Dentin caries.

A

A caries lesion into dentin

28
Q

▪Coronal caries.

A

A caries lesion in any surface of the anatomic tooth crown.

29
Q

▪Root caries.

A

A caries lesion in the root surface.

30
Q

▪Primary caries.

A

A caries lesion not adjacent to an existing restoration or crown.

31
Q

▪Secondary caries.

A

A caries lesion adjacent to an existing restoration, crown, or sealant. Other term used is caries adjacent to restorations and sealants (CARS). Also referred to as recurrent caries, implying that a primary caries lesion was restored but that the lesion reoccurred.`

32
Q

▪Residual caries.

A

Refers to carious tissue that was not completely excavated prior to placing a restoration. Sometimes residual caries can be difficult to differentiate from secondary caries.

33
Q

▪Cavitated caries lesion.

A

A caries lesion that results in the breaking of the integrity of the tooth, or a cavitation.

34
Q

▪Non-cavitated caries lesion.

A

A caries lesion that has not been cavitated. In enamel caries, non-cavitated lesions are also referred to as “white spot” lesions.

35
Q

▪Active caries lesion.

A

A caries lesion that is considered to be biologically active, that is, lesion in which tooth demineralization is in frank activity at the time of examination.

36
Q

▪Inactive caries lesion.

A

A caries lesion that is considered to be biologically inactive at the time of examination, that is, in which tooth demineralization caused by caries may have happened in the past but has stopped and is currently stalled. Also referred to as arrested caries, meaning that the caries process has been arrested but that the clinical signs of the lesion itself are still present.

37
Q

▪Rampant caries.

A

Term used to describe the presence of extensive and multiple cavitated and active caries lesions in the same person. Typically used in association with “baby bottle caries,” “radiation therapy caries,” or “meth-mouth caries.” These terms refer to the etiology of the condition.

38
Q

Striae of Retzius

A

Lines of incremental growth/bands seen in tooth enamel. They represent the incremental pattern of enamel, the successive apposition of different layers of enamel during crown formation.

39
Q

Mature plaque biofilm communities

A

Mature plaque biofilm communities have tremendous metabolic potential and are capable of rapid anaerobic metabolism of any available carbohydrates. The frequency of sucrose exposure for cariogenic plaque greatly influences the progress of tooth demineralization.
 C, In active caries, a progressive loss of mineral content subjacent to the cariogenic
plaque occurs.

40
Q

Direct tooth

A

Pellicle protects, ideal for bacteria to attach.If left undisturbed, biofilm rapidly builds up to sufficient depth to produce an anaerobic environment adjacent to the tooth surface.

41
Q

Best places for bacterial formations

A

Pits and fissures
 The smooth enamel surfaces immediately gingival to the proximal contacts and in the gingival third of the facial and lingual surfaces of the clinical crown
 Root surfaces, particularly near the cervical line
 Subgingival areas

42
Q

Radiolucency

A

greater transparency or “transradiancy” to X-ray photons. Materials that inhibit the passage of electromagnetic radiation are called radiodense or radiopaque, while those that allow radiation to pass more freely are referred to as radiolucent.

43
Q

Radiopacity

A

refers to the relative inability of electromagnetic radiation, particularly X-rays, to pass through a particular material. Radiolucency indicates greater transparency or “transradiancy” to X-ray photons.

44
Q

Root caries

A

Caries originating on the root is alarming because (1) it has a comparatively rapid progression, (2) it is often asymptomatic, (3) it is closer to the pulp, and (4) it is more difficult to restore.

45
Q

Xerostomia

A

After radiation, salivary glands become fibrotic and produce little or no saliva, leaving the patient with an extremely dry mouth, a condition termed xerostomia. Such patients may experience near-total destruction of the teeth in just a few months after radiation treatment. Salivary protective mechanisms that maintain the normal oral flora and tooth surface integrity include bacterial clearance, direct antibacterial activity, buffers, and remineralization.

46
Q

Saliva

A

While in the mouth, saliva lubricates oral tissues and bathes teeth and the biofilm.The secretion rate of saliva may have a bearing on caries susceptibility and calculus formation.
 Adults produce 1-1.5 L of saliva a day, very little of which occurs during sleep.
 The flushing effect of this salivary flow is, by itself, adequate to remove virtually all microorganisms not adherent to an oral
Salivary glands produce an impressive array of antimicrobial products. Lysozyme, lactoperoxidase, lactoferrin, and agglutinins possess antibacterial activity. These protective proteins are present continuously at relatively uniform levels, have a broad spectrum of activity, and do not possess the “memory” of immunologic mechanisms. The normal resident oral flora apparently has developed resistance to most of these antibacterial mechanisms.
 Although the antibacterial proteins in saliva play an important role in the protection of soft tissue in the oral cavity from infection by pathogens, they have little effect on caries because similar levels of antibacterial proteins can be found in caries-active and caries-free Individuals with decreased salivary production (owing to illness, medication, or irradiation) may have significantly higher caries susceptibility
The volume and buffering capacity of saliva available to tooth surfaces have major roles in caries protection. The buffering capacity of saliva is determined primarily by the concentration of bicarbonate ion. Buffering capacity can be estimated by titration techniques and may be a useful method for assessment of saliva in caries-active patients. The benefit of the buffering is to reduce the potential for acid formation.
 In addition to buffers, saliva contains molecules that contribute to increasing biofilm pH. These include urea and sialin, which is a tetrapeptide that contains lysine and arginine. Hydrolysis of either of these basic compounds results in production of ammonia, causing the pH to increase.
 Because saliva is crucial in controlling the oral flora and the mineral content of teeth, salivary testing should be done on patients with high caries activity. A portion of the salivary sample also may be used for bacteriologic testing, as will be described later in this chapter.

47
Q

Saliva - remineralization

A

Saliva and biofilm fluid are supersaturated with calcium and phosphate ions. Without a means to control precipitation of these ions, the teeth literally would become encrusted with mineral deposits. Saliva contains statherin, a proline-rich peptide that stabilizes calcium and phosphate ions and prevents excessive deposition of these ions on teeth.14 This supersaturated state of the saliva provides a constant opportunity for remineralizing enamel and can help protect teeth in times of cariogenic challenges.

48
Q

Diet

A

High-frequency exposure of fermentable carbohydrates such as sucrose may be the most important factor in producing cariogenic biofilm and, ultimately, caries lesions. Frequent ingestion of fermentable carbohydrates begins a series of changes in the local tooth environment that promotes the growth of highly acidogenic bacteria and eventually leads to caries. In contrast, when ingestion of fermentable carbohydrates is severely restricted or absent, biofilm growth typically does not lead to caries. Dietary sucrose plays a leading role in the development of pathogenic biofilms and may be the most important factor in disruption of the normal healthy ecology of dental biofilm communities. Because the eventual metabolic product of cariogenic diet is acid, and the acid leads to the development of caries, the exposure to acidity from other sources (e.g., dried fruits, fruit drinks, or other acidic foods and drinks) also may result in caries. The dietary emphasis must include all intakes that result in acidity, not just sucrose.