Pathogenisis Of Perio Disease

Front 1

OE continuous with JE

Back 1

Pristine gingiva

Front 2

Pristine gingiva %

Back 2

JE 10
CT 60
OE 30

Front 3

PMNs are present in pristine gingiva

Back 3

TRUE

PMNs are still present in healthy gums

Front 4

Compare JE to CT in pristine gingiva

Back 4

JE is thin

CT is dense

Front 5

subep loops vs dental plexus loops in pristine gingiva

Back 5

sub ep loops are constant

dentogingival plexus no loops

Front 6

initial lesion

Back 6

CLINICALLY HEALTY

Front 7

carbon particles leak out of vessels

Back 7

initial lesion

Front 8

transudate

Back 8

health

Front 9

exudate

Back 9

disease

Front 10

crevicular fluid

Back 10

flow rate increases with inflammation

Front 11

how do PMNs get to the sulcus

Back 11

through the JE

Front 12

bacterial chemo attractors

Back 12

LPS, fMetLeuPhe

Front 13

Vascular Events Initial lesion

Back 13

dialation
Increased permiability
gaps between capillary and endothelial cells
intercellular junctions close

Front 14

ICAM-1

Back 14

P selectin
CD 11 a

knocked out mice show decreased PMN migration

Front 15

ELAM-1

Back 15

CD62E

double knocked out mice show succeptibility to pyogenic bacterial infections

Front 16

Reasons for ginigival stability

Back 16

SEC APG

shedding
epithelial barrier
compliments
antimicro of antibodie
PMN and macrophages
GCF positive flow

Front 17

correlation of gcf to pmn in sulcus

Back 17

both increase similarly with plaque accumulation

Front 18

what part of JE is altered in initial lesion

Back 18

most coronal

Front 19

perivascular collagen loss

Back 19

Initial lesion

Front 20

cell to fiber ratio in healthy gingiva?

Back 20

low cell, high fiber

Front 21

early gingival lesion changes

Back 21

lymphocytes and PMNs increase

fibroblasts degenerate

Front 22

basal cells proliferate

rete pegs invade coronal epithlium

Back 22

early leasion

Front 23

when is lesion clinically visible

Back 23

early lesion

Front 24

what happens to capillary bed when JE invades CT

Back 24

opens up and proliferate into CT papille

Front 25

accumulation of lymphoid cells immediately below JE

Back 25

early leasion

Front 26

which IL do activated t cells produce

Back 26

2 3 4 5 6 10, 13 TNF alpha

Front 27

when do T B and plasma cells become evident

Back 27

established lesion

Front 28

what to plasma cells produce

Back 28

Igs and cytokines

Front 29

Fibroblasts produce

Back 29

MMPs and TIMPs

Front 30

What has happened to apical JE in established lesion

Back 30

NOTHING

Front 31

PE

Back 31

converted JE

not attached to tooth
loaded with PMNs

Front 32

switch from t cell to b cell dominance

Back 32

gingivitis to periodontitis

Front 33

first clinical sign of periodontitis

Back 33

destruction of CT root attachment and apical migration of JE

Front 34

where does bone loss occur

Back 34

around communicating blood vessels along crest of septum

Front 35

plasma cells >50%

Back 35

advanced lesion

Front 36

diabetes

Back 36

risk factor

Front 37

oral effects of diabetes

Back 37

xerostema
candida
periodontitis
perio abcesses

Front 38

Type 2 diabetes bacteria

Back 38

PI, CR, PG

Front 39

spirocytes

Back 39

increase in diabetes

increase in pregnancy

Front 40

Type I diabetes bacteria

Back 40

cap

Front 41

when is the best time to treat perio during pregnancy

Back 41

2nd trimester

Front 42

naphthoquiones

Back 42

form steroid used by PI

associatied with pregnancy

Front 43

direct estrogen response

Back 43

increase vascular permiability

decrease keratinization

decrease PME chemotaxis, and phagocytosis and Ab, T-cell responses

Front 44

lower GCF

decrease PMN function

increase keratinization

Back 44

smokers

Front 45

Papillon-Lefevre syndrome

Back 45

mutation in chromosome 11

Front 46

aggressive perio is hereditable

Back 46

TRUE

Front 47

increase perio succeptability in Caucasion

Back 47

IL-1