host responce in PDD/aetiolgy in PDD Flashcards
what do rete ridges do
prevent mobiltiy
junctional epitheliumis suceptible to
bacterial infection
bacterial produces can get access inaide tissue
why is junctional epithelium permeable
we need to secrete out into the OC
flattened cells
contain hemidesmosomes (contact BM)
pathologu of periodontal disease
saliva
epithelium
inflammatory responce
which antibody is found in saliva
secrety IgA
IgA
secreted as a dimer into OC through epithelial cells
- when being secreted a J chain attatches to it which links th emonomers together to form a dimer
what does IgA do to bacteria
bind to bacteria or products to stop its function
4 potential contact points
aggregates bactera
what does bacteria need to grow
iron
lactofrrin
compeititve inhbitor
binds to and sequesters free ion
binds LPS leading to formation of perioxide, increases bacterial membrane permeability
salivary thiocynate
enzyme
NADPH converted to hydrogen perioxoide, converted to HOSCN
is then coverted to hypothiocyanous acid in low amounts
types of antimicrobial proteisn
Defensins
Catholicidin peptides
Cathepsi C
Defensins
- Highly cationic membranes that insert into the bacterial membrane to create pores and bacterial cell lysis
catholicidin peptides
- punches holes in bacteria membranes in particular lipoprotein membranes(gram -)
cathepsin C roles
- serine protease released mainly by neutrophils
- degrades the outer membrane protein of bacteria
- activates other proteases via cleavage
- cleaves ECM components
role of eptihelum
desquamation means any bacteria is shed
permability barrier
junctional epithelium more permeable, sulcus bactera trapped
epithelum can stimulate immune responce and release cytokines
what is secreted from JE
gingival crevicular fluid
gingival crevicual fluid contains
C1-9
role of c3b
- inserts itself into the membranes of the bacteria
- leukocytes phagocytose it
C5-9
- membrane attack complex
- destroys microorganisms
- forms a channel pore to lyse the bacteria
C3a-C5a
- attract neutprhils and macrophages to the area(if complement is activated)
- vascular changes (increase permeability by the histamine)
- stimulate histamine release
- promote formation of leukotrienes and prostaglandins (pro inflammatory molecules)
- attract phagocytes by chemotaxis and aid phagocytosis via opsonisation
clotting cascade purpose
prevent spread to blood
fibrin forms a barrier to spread of infection
kininogens
- converted to kinins by proteases eg brady kinin
- acts very similar to histamine, promotes inflammatory respnce
- more serum and leukocytes into the OC due to vasodialtion
gingival crevicualr fluid limiatiosn
- bacteria in plaque can metabolise some components
- complement, immunoglobulin and other components partly consumed and degraded in crevice
how do neutrophils leave the blood stream
via extravasion and migrate towards site
attracted by chemokines
functions of neutrophils
phagocytosis
bind to complement receptors (opsonisation)
(if macrophage present will use MHC class II)
neutrophil function in PDD
production of Neutrophil extracellular traps
kill microbes by antimicrobial peptides
how do NETs work
- neutrophil will pick up and phagocytose as many bacteria as it can
- as they die (eaten as many bacteraia as possibke)they throw DNA strands, this will capture bacteria on the outside
- bacteria caught in the DNA strands
- macrophage can recognise and eat it
how do neutrophils attempt to remove biofilm
- secrete enzymes and NETS
- Kill bacteria and solublise plaque
- Washed out by GCF
chemokines funciton
- stimulate immune response
- release cytokines (drives inflammatory reponnsce)
- phagocytose
- stimulate healing (helps epithelium) if there is no permanet damage at this stage/no periodontits
tissue macrophages
Surveillance macrophages
- once the microbial load is too great they’ll respond
- secrete factors that recruit monocytes (blood) to the tissue
- then turn into macrophages into the tissue
what can macrophages do
- phagocytose
- antigen presenting
- secrete factors
- secrte factors which increase inflame repsonce
adaptive immune repsonce
1) Humoral immunity
- B cells
- Production of antibody by plasma cells
2) Cell mediated immunity
- T cells
- immune regulation and cytotoxic T cell killing of virally infected and neoplastic cells
what happens to bacteria which has been swallowed
- can be then associated with mucosal associated Lymphoid tissue
- Degraded in the stomach
- if not, in the intestines there are immune patches that have lymphoid tissue
- bacteria antigens can get taken up by the MALT^
- presented by dendritic cells/macrophages
- can then get B cell production of antibodies
- antibodies enter the serum and come out of the JE as the blood vessels there are very leaky
roles of antibodies in defence
- acts an opsonin
- activates neutrophil enzyme secretion (neutrophil degranulation)
- prevents bacterial attachment
- activates complement
antibodies and soluble factors
- neutralises toxins by binding to the active site
- inhibits enzymes (by binding to its active site)
chronic marginal gingivitus and characteristics
caused by expansion of the biofilm
Some of the enzymes attack the biofilm so much the tissue begins to be damaged)
Bleeding on probing (due to fragile tissue)
False pocketing
- due to swollen gingiva but functional epithelium still attached
Junctional epithelium still attached
- Gingivitis is reversible
- alveolar bone is still intact
destructive periodonttis
Complete breakdown
- alveolar bone broken down
- not reversible
periodontal pocket
- pathologically deepened gingiva sulcus that may occur by coronal movement of the gingiva margin apical displacement of gingiva attachment or both
cause of tissue damage and bone loss in periodotnal disease
bacteria products
host products
bacteria products which damage bone and tissue
1) Endotoxins
- may damage epithelium
- fibroblasts
2) Bacterial enzymes
- collagenase
- hyaluronidase
- gingipains break down the connective tissue
3) Lipopolysaccharide, capsular material, peptidoglcans,muramyl dipeptide, proteases may cause bone resorption
host products which cuase tissue and bone loss
1) Release of enzymes from neutrophils
- damaging cell tissues
- negative feedback tissues on our own issues
2) complement
3) production of IL-1, IL-6 by macrophages
- stimulates bone resorption and epithelial proliferation
- tries to drive an inflammatory responce
4) Inflammatory mediators
- prostaglandins
- other cytokines
- leukotrienes
also stimulates bone resorption
