general Flashcards

(30 cards)

1
Q

Most reliable study design ?
Most common study design ?

A
  1. Randomized controlled trials<br></br>2. Case-control and cohort studies 
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2
Q

Define prevalence

A

Number of individuals that have a particular condition within a defined population

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3
Q

Define: Odds

A

the probability that an event happened divided by the probability that an event did not happen.

often easier to estimate than probability, so often reported in studies

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4
Q

Risk?

A

Probability that an individual or a site will develop a particular condition or disease during follow-up.
When risk is reported, it should be accompanied by a specific time period.

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5
Q

Who is the father of dentistry?

A

Pierre Fauchard

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6
Q

What’s the maximum distance between bone fragments that allow for direct bone healing?

A

direct healing <800 µm
* contact healing: no gap is present (direct cortical contact)
* gap healing: in stable gaps with a width >200 µm osteonal diameter but <800 µm

indirect bone healing: areas with large gaps (>800 µm) or without this degree of rigid fixation

Source: Verstraete book chapter 2

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7
Q

Verstraete, ed 2, chapter 2.

how much osteoid can osteoblasts produce per day?

A

A layer of 1 µm of osteoid (organic matrix of bone) may be produced per day, followed by a maturation phase of 10 days before calcification

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8
Q

Verstraete, ed 2, chapter 2.

what is the difference between woven and lamellar bone regarding their microscopic structure?

A
  • Woven bone: randomly oriented collagen fibrils
  • Lamellar bone: collagen fibrils are arranged in parallel bundles
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9
Q

Verstraete, ed 2, chapter 2.

how much bone can osteoclasts resorb per day?

A

50–100 µm bone per day

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10
Q

Verstraete, ed 2, chapter 2.

define direct and indirect bone healing. under what conditions does each of them occur?

A

direct healing: Callus-free (only bone forms), requires
“absolute stability by interfragmentary compression”.
* Direct healing, contact healing: no gap is present (direct cortical contact), between compressed bone fragments, either adjacent to the plate (cis cortex) or where interfragmentary compression can be applied.
* Direct healing, gap healing: In stable gaps with a width of >200 µm osteonal diameter, but <800 µm. Usually observed far from the fixation (the opposite bone cortex) or in areas where interfragmentary compression is not obtained

indirect bone healing: areas with large gaps (>800 µm), or without rigid fixation. a callus is formed (fracture -> hematoma -> granulation tissue -> cartilage -> fibrocartilage -> woven bone -> lamellar bone).

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11
Q

Assessment of Dental Pathology Using Visual Oral Examination in 1082 Dogs in Türkiye. Melike Kübra Adak, Ibrahim Akin. JVD 2025.

What was the effect of wet diet on observed dental disease status?

A

Wet diet worse for all teeth in the study

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12
Q

“Assessment of Dental Pathology Using Visual Oral Examination in 1082 Dogs in Türkiye”. Melike Kübra Adak, Ibrahim Akin. JVD 2025.

What was the effect of a dry diet on specific teeth

A
  • dogs fed dry food had lower than expected disease presence in canines and premolars
  • dogs fed homemade food showed lower disease prevalence in canines and molars compared to the expected levels
  • dogs on a mixed diet had a higher disease prevalence in canines and premolars compared to the expected levels
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13
Q

Assessment of Dental Pathology Using Visual Oral Examination in 1082 Dogs in Türkiye. Melike Kübra Adak and Ibrahim Akin. JVD 2025.

What was the effect of a home cooked diet on specific teeth?

A

Home cooked diet showed less observed disease on the canines and molar teeth

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14
Q

Junctional epithelium as a function of attaching to the tooth?

A

Unique epi structure surface cells are specialized to attach to the tooth, so unlike other epi cells in body, it cannot slough.
Cells at basal layer continually divide and move to within 2 or 3 cell layers of the tooth surface and then migrate coronally, parallel to the tooth surface to eventually reach the floor of the sulcus to be sloughed off in the gingival crevice.

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15
Q

extracellular spaces of junctional epi compared to other epi?

A

Extracellular spaces b/w the junctional epi are greater than other tissues, with intercellular spaces comprising about 18% of the volume.

Making junctional epi LEAKY

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16
Q

How does the epithelium play an active role in innate immunity?

A

by expressing antimicrobial peptides, called defensins -secrete chemokines to attract neutrophils.

17
Q

Healing after periodontal therapy: regeneration vs repair?

A
  • regeneration: growth from the same type of tissue that has been destroyed.
  • repair: restores continuity of the diseased marginal gingiva and reestablishes a normal gingival sulcus.
18
Q

Host modulation therapy
What is it
What are commonly used to do it?

A

“Host modulation therapy (HMT) is a therapeutic strategy—most commonly used in periodontology—that targets the patient’s inflammatory and immune response, rather than (or in addition to) directly targeting the microbial biofilm.”

NSAIDS
* inhibit prostaglandin formation (PGE2) by neutrophils, fibroblasts, macrophages, and epi cells in response to bacterial LPS
* PGE2 upregulates bone resorption by osteoclasts and inhibits fibroblast fxn (which modulates immune response)
* Use has not taken off because of side effects

bisphosphonates
* inhibit bone resorption by disrupting osteoclast activity
* possess anticollagenase properties and interfere with osteoblast metabolism and secretion of lysosymal enzymes
* unwanted effects include inhibiting bone calcification and inducing changes in WBC counts, also, avascular necrosis of jaws

Sub-antimicrobial dose doxycycline
* exerts its effect by enzyme, cytokine, and osteoclast inhibition (not antibiotic!)

19
Q

Wiggs, chapter 10.

Gingival curettage vs subgingival curettage?
Healing after curettage?

A
  • Gingival curretage: removal of the inflamed soft tissue lateral to the pocket wall and the junctional epi.
  • Subgingival curretage: performed apical to the junctional epi and severing the connective tissue attachment down to the alveolar crest.

need to remove inflamed granulation tissue is questionable.

Healing after curretage:
* restoration and epithelialization of the sulcus require 2-7 days
* restoration of the junctional epithelium occurs in animals as early as 5 days after treatment
* immature collagen fibers appear within 21 days

20
Q

Internal bevel incision benefits?

A
  • removes pocket lining
  • conserves the relatively uninvolved outer surface of the gingiva
  • produces a sharp, thin flap margin for adaptation to the bone-tooth junction
21
Q

Is protein content of GCF correlated to level of disease?

22
Q

In clinically normal gingiva of humans, what is the basis of inflammatory cells?

A

Mostly T cells, very few B cells or plasma cells

23
Q

How do established gingivitis lesions progress?

A

Some remain stable and do not progress over months or years!
Some become more active and convert to destructive lesions.

24
Q

Histologic evaluations on animal specimens revealed that in early stages of gingivitis, what is ubiquitous?

A

expression of cytokines responsible for connective tissue breakdown (MMPs!)

25
How does gingivitis differ in children vs adults?
Response in children is dominated by T cells (not B cells), very few plasma cells. Could explain why gingivitis in children rarely progresses to periodontitis.
26
Healthy gingiva is associated with what microorganisms? diseased gingiva?
* mostly coccoid cells and straight rods * increased numbers of spirochetes and motile rods
27
explain the gradual movement of the pocket
PMNs invade the coronal aspect of junctional epi due to inflammation, once these occupy about 60%, the tissue detaches from the tooth surface. At the same time, as a result of collagen destruction, the apical cells of the junctional epi proliferate along the root, resulting in an apical shift.
28
Extension of junctional epi along the root requires?
healthy epithelial cells! If there is necrosis of the junctional epi, this impairs pocket formation and ulcerative gingivitis results
29
Is bone destruction in periodontal disease a function of bone necrosis? How does bone destruction progress in periodontal disease?
NO! It involves the activity of living cells along viable bone bacterial plaque products induce differentiation of bone progenitor cells into osteoclasts and stimulate gingival cells to release mediators that have the same effect. Plaque products and inflammatory mediators can also directly inhibit osteoblasts.
30
Even in healthy gingiva, there are always what?
inflammatory cells, particularly neutrophils, also lymphocytes and macrophages.