pathogenesis of periodontitis Flashcards
why would someone have gingival health
Superb hygiene
hows the Junctional epithelium in gingival healtyh
attached to enamel
how does the oral epithelium and the Junction epithlium relate in gingival health
Looks continues
Inflammation in gingival health
Virtually absent
tissue volume ratio in health
10% JE
30% OE
60% CT
what immune cells are present in gingival health
Few PMNs present in the outer portion of the JE
thickness of junctional epithelium in health
Thin (10-20 cell layers
are epithelial ridges present in JE during healtyh
Absent
how does the CT look in gingival healthy
Dense with prominent collagen fiber bundles
what do the vapillaries look in the subepithelial plexus in gingival health
has loops that are constant
what do the capillaries look like in the dentogingival plexus in health
No loop
why does clinically healthy gingiva remain stable
Shedding of epithelial cells Intact epithelial barrier Positive flow of GCF complement system PMNs and macrophages Protective effects of antibodies
why does the subepithelial plexues capillary loops go through the retee pegs
Get nutrients and O2 to the epithlium
what is the subclinical stage of gingivitis
Initial lesion
what is the clinical early stage of gingivits
Early lesion
what is chronic gingivitis(no bone loss yet)
Established lesion
what is the stage that is the progression to periodontitis (bone loss)
Advanced lesion
when does the inital lesion occur
within 1-4 days of plaque development
what does the increased permeability of an inital lesion lead to
Carbon particles and serum proteins leak out of vessels
what does infiltration show in the inital lesion
PMNs and monocytes in the JE
lymphocytes in the CT (5%)
what happens to the vessels in the inital lesion
Vascular density
what happens to collagen in the inital lesion
Decreased perivascular colagen
what happens in the gingival crevicular fluid volume in the initial lesion
Increases
can you clinically see the inital lesion
No
what normally can pass through a vessel
Water
salts
small molecules
how do intercelular junction look in an intial lesion
Normally closed
what causes dilation of vessels of the dentogingival plexues
Vasoactive mediators
histamine, IL-1, TNF
what does gaps forming from dialtion of vessels lead to
Increased permeability
fluid and prtein flow out
GCF flow increases
White blood cells can leave
what is Gingival crevicular fluid made of
Plasma transudate (health) inflammatory exudate (disease)
what does gingival crevicular fluid pass through to get to crevis
Through the periodontal tissues
what does the GCF constituents indicate
Inflammatory changes
bacterial colonization
what causes GCF flow rate to increase
Clinical inflammation
what is used to measure GCF volume
Ninhydrin stain for protein
what mediates the up-regulation of adhesion molecules on endothelial cells in an initial lesion
Cytokine mediated
what does the adhesion moelcules of endothelial cells in an intiial lesion do
Allows PMN’s to adhere to post-capillary venules
- migration
where do PMNs migrate in an inital lesion
Through JE into gingival sulcus
what induces chemotaxis by PMNs
Host factors (Il-8, C5a) Molecules released by bacteria (fMetLeuPhe)
what happens to the JE in the inital lesion
Alteration of the most coronal portion of the JE
when does an early lesion tend to occur
within 4-7 days of plaque development
what immunologic cells appear in the Early lesion
Lymphocytes and PMNs subjacent to JE
Few Plasma cells
how much of the infiltrated connective tissue is there
15%
what happens to the fibroblasts in an early lesion
Undergoing cytopathic alterations
can you see inflammation in early lesions
yes, clinically evident
what happens to the Collagen in early lesions
Destroyed
- creates space for infiltrate
what happens to basal cells in an early lesions
Cells of JE and SE proliferate
rete pegs invade the coronal portion of the lesion
what happens to the Dentogingival plexues
- Dilated w/ venules
- extremely permeable following minor trauma or inflammation
what happens as JE invades the CT
preivously inactive capillary bed opens up and proliferates into the CT papillae
why does junctional epithelium proliferate in early lesiosn
to compensative and fight plaque
what cells are present in an early lesion
Macrophages
T cells
B cells
Firboblasts
what is clinically seen in an established lesions
increased swelling
what hapens to crevicular fluid in established lesion
increased fluid exudation
what cells tend to migrate in an established lesion
leukocyte migration
plasma cell increased around blood vessel in coronal CT
what happens to the collagen in established lesion
loss continues as infiltrate expands
what cells become present in an established lesion
Macrophages and serum proteins
T and B cells
Plasma Cells
What do activated T cells Produce in an established lesion
Cytokines (IL-2, 3, 4, 5, 6, 10 , and 13, TNF-alpha) Chemotactic substances (MCP, MIP, and Rantes)
what do plasma cells produce in an established lesion
Produce Ig and Cytokines (IL-6 and TNF-alpha_
what do fibroblasts produce in an established lesion
MMPs and TIMPs
what happens to the JE and Sulcular epithelium in an established lesion
Proliferate and migrate deep into CT
what happens to the sulcus in an established lesion
deepens
what happens to just JE during an established lesion
JE converted into permeable pocket epithelium
what are characteristics of PE
not attached to tooth surface
Loaded with PMNs
what is an established lesion look like pathologically
Chronic gingivitis
how does the margin look like in an established lession
Rolled gingival margin
lots of redness
bleed on probing
is there attachment lost in an established lession
No
- probe depth increased but no attachment loss
how can one fix an established lession
clearing plaque
when does an advanced lesion occur
Not well known
how do cells change in an advanced lesion
switch from T to b cell prodminance
-converstion from gingivitis to periodontitis
what happens to the CT attachment in an advanced lesion
Destruction of CT attachment to root surface
what is the first clinical sign of periodontitis
migration of epithelail attachment indicates
where does bone loss begin in an advanced lesion
begins around communicating blood vessels
along crest of septum
what does the PE proliferate into an advnaced lession
Deep into CT
is the PE attached to the tooth in an advanced lession
Not attached
what is the most common cell in advnaced lesion
50% plasma
are there lots of cytokines in in advanced lession
Small spectrum of pro-inflammatory cytokines
what happens if you clear plaque from an advanced lession
basal and epithelium have signal die away
- may not get all your attachment back
Common modify factors of advanced lession
Diabetes
Pregnancy, pubery, and menopause
Smoking
modifying factors can influnce what
Susceptibility to gingivitis and periodontitis Plaque growth and composition Clinical presentation Disease progression Response to periodontal therapy
how can diabetes mellitus be a risk factor for oral and periodontal problems
Xerostomia
Candida infections
Periodontitis
Multiple periodontal abscesses
how much control should you have over diabetes
good control will lead to less periodontitis
- poor control=problems
what does periodontitis do for diabetes
increasees insuline resistance
have a higher incidence of proteinuria and cardiovascular problems
what happens in diabetteics after periodontal therapy
Glycemic control improved
how can diabetes affect periodontis
change the bacteria
change host response
efect on periodontal treatement
what effect on the host response can diabetes have
PMN fuction. chemotaxis impaired
cytokines, monocytes, and macrophages
Connective tissue
what can diabetes affect in treatment
poorly controled leads to poor results
what effect does estrogen have on periodontitis
Affects salivary peroxidases
increases collagen metabolism and angiogenesis
how does pregnancy affact periodontium
increase estrogen
increase vascular response and inflammatory mediates
gingival inflammation increase
increase in gingival bleeding during menstrual cycle
how common is gingivitis in pregnancy
35-88%
when is pregnancy related gingivitus most common
2nd and 3rd trimesters
what is the second risk factor for periodontitis
Smoking
what does tobaccco smoking cause in perio
Deeper pockets
more attachmnet loss
more tooth loss
less bleeding on probing
what can smoking affect
Bacteria
Host
how does smoking affect reattachment for treatment
Poorer reduction in probing depth
poorer attachment gain in nonsurgical treatment
what happens to treatment if you quite smoking
BEtter treatment outcome
