Surface coatings of the tooth Flashcards
what makes up nasmyths membrane
reduced enamel epithelium + primary enamel cuticle
2 cell layers that make up the reduced enamel epithelium
ameloblasts (flattened, post maturation stage)
stratum intermedium
(both parts of the ENAMEL ORGAN
define primary enamel cuticle
basal lamina associated with reduced enamel epithelium and the newly formed enamel surface
what produces the primary enamel cuticle
mature ameloblasts
describe nasmyths membrane and when it is present
covering over tooth once enamel has formed, pre eruption only
describe what happens in reduced enamel epithelium during eruption
stratum intermedium divides –> REE thickens to meet overlying oral epithelium= PRIMARY JUNCTIONAL EPITHELIUM
what joins reduced ameloblasts to the basal lamina (primary enamel cuticle)
hemidesmosomes
what forms junctional epithelium
mostly REE (stratum intermedium) small amount from oral epithelium (determined by cytokeratin expression patterns)
how/ what does primary epithelium change in to
moves down tooth surface as tooth erupts –> JE rests at last apical mms of enamel = SECONDARY JUNCTIONAL EPITHELIUM
function of JE what happens when it fails
BARRIER seals oral environment from underlying connective tissues (forms collar whole way around tooth)
(breach –> periodontal disease
where is JE in relation to gingival sulcus
top of JE –> bottom of gingival sulcus
what happens to JE position in periodontal disease
moves down tooth –> attaches to cementum instead of enamel –> increased length of sulcular epithelium
where is junctional epithelium thickest
nearest the oral cavity
may only be 1-2 cells thick nr cementum
structure of junctional epithelium
stratified, non-keratinised epithelium
4 reasons junctional epithelium is unique
- 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
location of JE’s 2 basal lamina
UNIQUE; DOESNT MATCH:
internal basal lamina IBL –> Enamel
External basal lamina –> Connective tissue
how does JE basal lamina attach to enamel surface
hemidesmosomes
how does the junctional epithelium attach to the IBL
DAT cells (directly attaching cells)
what is bullous pemphigoid protein
one of the proteins that attaches JE DAT cell to IBL
describe/ explain bullous pemphigoid disease
autoimmune condition –> attack on bullous pemphigoid antigens –> cells separate from basal lamina –> fluid filled ulcers on skin and oral mucosa
explain the funnel effect
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
evidence that funnel effect helps prevent infectino
neutrophils (and nerve endings) also present in JE interceullular spaces (migrating up for desquamation) in dogs and rats
compare rate of turnover of JE to oral mucosa
50-100x faster
4 ways JE prevents infection 8
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
where do nerve cells in JE originate
connective tissue
what do JE nerve endings contain 2
- substance p
- calcitonin gene related peptide (CGRP)
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
what is region where most bacteria invading JE come from and why
enamel in gingival sulcus- difficult to access w toothbrush
rate of flow of PMNs/ minute through JE
30,000
where do neutrophils/ PMNs etc (outward GCF flow) originate
connective tissue around tooth
how do the intercellular spaces enlarge
- rupture of (modified) desmosomal junctions
- distended by PMNs and fluid
how often are no inflammatory cells found in JE
never/ vv rare
amount of GCF found in health
none/ very little
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)
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
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
function of AEP 2
- lubricating layer for efficient mastication
- prevents oral tissue dehydration
how does plaque form
oral bacteria adhere to AEP
how does dental biofilm form
AEP + plaque
