Surface coatings of the tooth Flashcards

1
Q

what makes up nasmyths membrane

A

reduced enamel epithelium + primary enamel cuticle

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2
Q

2 cell layers that make up the reduced enamel epithelium

A

ameloblasts (flattened, post maturation stage)
stratum intermedium
(both parts of the ENAMEL ORGAN

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3
Q

define primary enamel cuticle

A

basal lamina associated with reduced enamel epithelium and the newly formed enamel surface

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4
Q

what produces the primary enamel cuticle

A

mature ameloblasts

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5
Q

describe nasmyths membrane and when it is present

A

covering over tooth once enamel has formed, pre eruption only

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6
Q

describe what happens in reduced enamel epithelium during eruption

A

stratum intermedium divides –> REE thickens to meet overlying oral epithelium= PRIMARY JUNCTIONAL EPITHELIUM

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7
Q

what joins reduced ameloblasts to the basal lamina (primary enamel cuticle)

A

hemidesmosomes

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8
Q

what forms junctional epithelium

A
mostly REE (stratum intermedium)
small amount from oral epithelium (determined by cytokeratin expression patterns)
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9
Q

how/ what does primary epithelium change in to

A

moves down tooth surface as tooth erupts –> JE rests at last apical mms of enamel = SECONDARY JUNCTIONAL EPITHELIUM

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10
Q
function of JE
what happens when it fails
A

BARRIER seals oral environment from underlying connective tissues (forms collar whole way around tooth)
(breach –> periodontal disease

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11
Q

where is JE in relation to gingival sulcus

A

top of JE –> bottom of gingival sulcus

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12
Q

what happens to JE position in periodontal disease

A

moves down tooth –> attaches to cementum instead of enamel –> increased length of sulcular epithelium

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13
Q

where is junctional epithelium thickest

A

nearest the oral cavity

may only be 1-2 cells thick nr cementum

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14
Q

structure of junctional epithelium

A

stratified, non-keratinised epithelium

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15
Q

4 reasons junctional epithelium is unique

A
  • has 2 basal lamina
  • wide intercellular spaces (modified desmosomes, no tight junctions)
  • only barrier that is not KERATINISED (eg compared to skin)
  • best turnover of any tissue; all cells in JE turnover, not just basal layer
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16
Q

location of JE’s 2 basal lamina

A

UNIQUE; DOESNT MATCH:
internal basal lamina IBL –> Enamel
External basal lamina –> Connective tissue

17
Q

how does JE basal lamina attach to enamel surface

A

hemidesmosomes

18
Q

how does the junctional epithelium attach to the IBL

A

DAT cells (directly attaching cells)

19
Q

what is bullous pemphigoid protein

A

one of the proteins that attaches JE DAT cell to IBL

20
Q

describe/ explain bullous pemphigoid disease

A

autoimmune condition –> attack on bullous pemphigoid antigens –> cells separate from basal lamina –> fluid filled ulcers on skin and oral mucosa

21
Q

explain the funnel effect

A

proliferative cell layer next to connective tissue –> new cells in JE–> migrate coronally due to 3:

  • wide intracellular spaces
  • no tight junctions
  • modified desmosomes
  • -> desquamation of cells to gingival sulcus = GINGIVAL CREVICULAR FLUID
22
Q

evidence that funnel effect helps prevent infectino

A

neutrophils (and nerve endings) also present in JE interceullular spaces (migrating up for desquamation) in dogs and rats

23
Q

compare rate of turnover of JE to oral mucosa

A

50-100x faster

24
Q

4 ways JE prevents infection 8

A

DNT Let Fucking Paedos Near Children

  • Desmosomes modified, less than other tissues
  • Neutrophils intercellular (dogs/ rats) (GCF, funnel effect)
  • Turnover is rapid
  • Lysosomal bodies in JE cells (acid phosphatase activity, engulf bacteria and cellular debris)
  • Funnel effect (bidirectional flow of GCF and cells as antimicrobial defense mechanisms)
  • Physical barrier via intercellular adhesion molecules
  • Nerve endings modulate JE cells and neutrophils
  • Cytokine expression
25
where do nerve cells in JE originate
connective tissue
26
what do JE nerve endings contain 2
- substance p | - calcitonin gene related peptide (CGRP)
27
what moves in each direction of bidirectional flow of GCF
out: neutrophils/ PMNs, JE cells, fluid exudate from connective tissue in: bacteria from oral cavity/ enamel surface
28
what is region where most bacteria invading JE come from and why
enamel in gingival sulcus- difficult to access w toothbrush
29
rate of flow of PMNs/ minute through JE
30,000
30
where do neutrophils/ PMNs etc (outward GCF flow) originate
connective tissue around tooth
31
how do the intercellular spaces enlarge
- rupture of (modified) desmosomal junctions | - distended by PMNs and fluid
32
how often are no inflammatory cells found in JE
never/ vv rare
33
amount of GCF found in health
none/ very little
34
4 sources of GCF constituents + examples
1 IN ORAL CAVITY: microbial plaque (LPS, enzymes, metabolic end-products) 3 IN CONNECTIVE TISSUE: -host inflammatory cells (PMNs, leukocytic enzymes, lactoferrin, lysozyme) -host tissue (collagens, proteoglycans, matrix proteins -serum derived factors (IgGs, complement, cytokines, eicosanoids, prostaglandins, leukotrienes)
35
formation of acquired enamel pellicle
post eruption: REE and underlying primary cuticle (Nasmyth's membrane) break down by attrition/ abrasion --> acquired enamel pellicle forms in its place
36
2 layers/ contents of AEP
- Acellular base layer (protective proteins strong bind to HA) - Organic matter from 3: saliva (statherin, proline-rich proteins), bacteria, GCF
37
function of AEP 2
- lubricating layer for efficient mastication | - prevents oral tissue dehydration
38
how does plaque form
oral bacteria adhere to AEP
39
how does dental biofilm form
AEP + plaque