histo/pathogensis of perio diseas :) Flashcards
normal periodontoum
bone
PDL
Gingiva
cementum
what lines the root surace
cementum
gingival epithelium histology
long rate ridges
junctional epithelium
thinner and more porous
forms barrier against dentinal plaque
attaches at the CEJ
healthy periodontium
junctional epithelium attaches at the ACJ
PDL attaching to alveolar bone
protective features of the host against PDD
barrier effect of intact junctional epithelium
factors in saliva
gingival crevicular
activation of T/B cells
gingival crevicular fluid
originates from gingival capillaries
contains neutrophils and complement
risk factors of PDD
poor oral hygiene
smoker
genetic
systemic disease
gingivitis symptoms
vasodilation increased blood flow damage to fibroblasts oedema increase in crevicular fluid still in tact at ADJ
histological changes at gingivitis
hyperplasia of JE increased inflammatory cells no migration of JE or bone loss increased blood flow loss of gingival collagen fibres development of deeper rate ridges more inflammatory cells junctional epithelium still attaches to ADJ
clinical changes of gingivitis
bleeding on probing
false pocketing
pain, redness, swelling
pre disposing factors to gingivitis
- Pregnancy/puberty
- Orthodontic appliances
- Dentures
- Restorations with overhangs
- Effects of medications
periodontist symtoms
JE has moved apically
plaque has moved more apically bone loss
more inflammatory cells
clinical changes of periodontitis
tooth mobility true pocket over 4mm bleeding on probing recession tooth loss halitosis calculus junctional epithelium may ulcerate
periodontisis histology
junctional epithelium ends more apically than at ADJ
true pockett formed
more inflammatory cells
BPE scoring
code 0-4
* furcation involvement
where can growth of plaque be
supra or sub gingival
what is growth on the tooth called
biofilm
what is a biofilm
3D structure of heterogenous bacterial and the material produced as a product of growth
subginigval plaque
heterogenous
firmly attached bacteria at tooth surface
many different cocci and bacilli
channels can run in the 3D structure allowing nutrients to flow
bacteria in a periodontal pocket
contains mainly gram positive Layer attached to hard tissue
overlying gram - layer
many motile and anaerobic bacteria
progression to periodontist
not always precede by gingivitus
early lesion can take many years to progress to advanced lesion, signifies change from gram + to gram - bacteia
what changes a quiescent site to an active one
change in host
change in microbial challenge
dysbiosis
healthy to disease
what do gram - and aerobic bacteria produce
short fatty acids
keystone pathogens
red complex bacteria can alter the community to move it to a disease causing community
produce virulence factors
what do the red complex bacteria do
produce virulence factors
change in complement levels changes immune repsonce
bacteria grow, leading to more inflammation
rapidly processing periodontal disease
produces LtA leukotoxin that targets neutrophils
CDT toxin that targets epithelial cells
acute necoritising ulcerative gingivitis
true infection with tissue invasion
associated with identifiable predisposing factors
what causes acute necrotising ulcerative gingivitis
small selection of specific bacteria by host derive nutrients
fuso-spirochaetal complex
pathogenic community at host interface
removes sugars from human cells
cytokines being produced by antigens produced by bacteria
community stick together, communicate with each other
produce different virulence factors
what are all the community pathogenic factors leading to a disease community
- LPS and capsule
- fibronectin
- toxins
- anaerobic growth proceeds butyric acid
- phospholipase digests lipids, glucosidases digest glycoproteins removing sugar so organisms can grow
what do LPS and capsule do to contribute to the disease coomunit
cause immune responce stimulating cytokine production
what does fibronectin do in contributing for community pathogenic factors
allows sticking to surfaces
