DP02 pathogenesis and histology of perio Flashcards
(26 cards)
What local factors affect development of perio?
Anatomy of teeth
Restorations
Alignment
Occlusal relations
Anatomy of the gingiva and alveolar bone
What systemic factors affect development of perio?
Diseases: Diabetes mellitus, blood diseases
Pregnancy and sex hormones: oestrogen, progesterone
Nutrition: scurvy, protein deficiency
Drugs: phenytoin, cyclosporin, ibuprofen, indomethacin
Immunological status: AIDS
Habits: smoking/chewing tobacco
What is the aetiology of perio?
Plaque (not amount)
Age
(immune response)
What bacteria are found in healthy gingiva?
More aerobic, gram +ve, non-motile
Eg streptococcus, actinomyces, veillonella
What bacteria are found in chronic gingivitis?
A bit more addition of gram -ve and positive and some motile rods
+fusobacterium
Prevotella
What bacteria are found in chronic perio?
Higher % of anaerobic, more gram -ve, more motile rods
Eg P gingivalis, F nucleatum etc Spirochaetes
What is the histology of the epithelium of healthy perio tissues?
Dermal papillae CT underlying rete pegs
Junctional epithelium is very thin and has no rete pegs
What is the histology of the epithelium in unhealthy perio tissues?
Proliferation in sulcular epithelium –> rete pegs and chronic inflammatory cells seen. JE attaches to cementum rather than enamel.
If plaque extends into the sulcus –> inflammatory response –> induces cell proliferation –> rete pegs seen
There are 4 stages in the transition from health to periodontitis. Describe the initial lesion - initial gingivitis - CLINICAL FEATURES
2 to 4 days after plaque accumulation
No clinical features
There are 4 stages in the transition from health to periodontitis. Describe the initial lesion - initial gingivitis - HISTOLOGICAL FEATURES
→ Acute inflammatory changes
Vasodilation
Fluid exudation and crevicular fluid
Cellular exudation of polymorphonuclear (PMN) cells
→ Enhanced transmigration of PMN cells
→ Disruption of intercellular spaces of junctional epithelium: impairment of barrier function
Desmosomes/hemidesmosomes disrupted
There are 4 stages in the transition from health to periodontitis. Describe the early lesion - early gingivitis
4 - 7 days after plaque accumulation
Exacerbation of the initial lesion
Further impairment of barrier function
→ Disruption of intercellular spaces
→ Failure to maintain attachment to enamel
→ Deepening of the gingival sulcus -> subgingival plaque
Anaerobic environment -> more anaerobic bac
Lymphocytic infiltration
Chronic inflammatory cells - lymphocytes and plasma cells
Cytopathic changes in gingival fibroblasts -> no longer produce collagen
Loss of collagen
Hyperplasia of junctional epithelium -> rete ridge formation
There are 4 stages in the transition from health to periodontitis. Describe the established lesion - established gingivitis
2 - 3 weeks after plaque accumulation
Exacerbation of the initial lesion
→ Expansion of the volume of tissue involved
→ Increase in disruption and hyperplasia of junctional epithelium
→ Ulceration of gingival pocket epithelium
Ulceration = loss of cells
In this case strat. sq. epithelium - all layers lost so CT exposed to pocket space -> no more barrier
In these areas of ulceration, there is loss of GCF exudation and BOP
→ Increase in plasma cell infiltration (B), decrease in lymphocytes (T)
→ Continued destruction of connective tissue
Varying attempts to repair: hyperplastic gingivitis
Vol of gingiva increases - pocket seems deeper than it actually is
Should remove plaque and have px return in 2 wks -> record pocket depth
There are 4 stages in the transition from health to periodontitis. Describe the advanced lesion - chronic periodontitis
Extension of inflammation beneath the base of the JE
Plasma cell infiltration, some lymphocytes & macrophages
→ Destruction of supra alveolar collagen, loss of attachment to cement
→ Apical migration of junctional epithelium
→ Pocket formation
→ Osteoclastic resorption of alveolar bone
What things can ulceration in established gingivitis be induced by?
Exotoxins, endotoxins, hydrolytic enzymes
How do exotoxins, endotoxins and hydrolytic enzymes induce ulceration in established gingivitis?
→ Exotoxins
EC toxic substances (proteins) liberated by bac
→ Endotoxins
Lipoproteins/polysaccharide complexes liberated by bac cell wall breakdown (toxic)
Cause severe inflammatory response
→ Hydrolytic enzymes
Increase epithelial permeability more than tissue breakdown but allow entry of other enzymes that may cause tissue destruction
In established gingivitis the ECM of CT is destroyed, describe the balance between decreased synthesis and increased degradation.
Decreased synthesis - Cytopathic changes in fibroblasts occur -> less collagen production
Increased degradation -Exogenous (bac) and endogenous (inflammatory cells/lysosomes/fibroblasts) proteases/collagenases; phagocytosis
What is horizontal bone loss characterised by?
Suprabony pockets
What are suprabony pockets?
Deepest part of pocket above alveolar bone crest
These pockets have one soft wall (gingiva) and one hard wall (tooth surface)
What is vertical bone loss characterised by?
Infrabony pockets
What are infrabony pockets?
Deepest part of pocket below alveolar bone crest
These pockets will have two hard walls (bone and tooth surface)
What are the local mediators involved in bone resorption?
Cytokines - IL1 IL2 TNF
Prostaglandins - PGE2
Growth factors - from osteoblasts - regulate osteoclast recruitment
What is the normal distance from the CEJ to bone crest?
2mm
(general increased observed with age)
What is the pathogenetic mechanism of perio disease?
- Disturbance in host-parasite relationship
- Activation of host inflammatory and immune response
- Enhanced synthesis of inflammatory mediators
- Burst of breakdown of CT/bone
- New eqm in host-parasite relationship as host manages the challenge from plaque bac [remission]
Why does herpes simplex virus hide in the trigeminal ganglion?
Neurones here do not express Class I histocompatibility complexes which cells display when they have been infected to alert the immune system
