Gingivitis is an inflammation of the gingival tissues. In early gingivitis there are increased levels of PMNs, T cells, immunoglobins and complement. There is only collagen loss in the infiltrated connective tissue. In established gingivitis, a pseudopocket is formed, with elevated GCF levels, plasma cells. There is further collagen loss and fibroblast damage.
At this stage there are many pro-inflammatory cytokines present, as well as PGE2, TNF.
After awhile, if the gram-negative bacteria in the plaque are present, and the host response is inadequate or inappropriate, periodontal destruction will begin. In this, there are elevated levels of macrophages which, as we know, can mediate the production of pro-inflammatory cytokines, oxygen radicals, and PGE2. These can stimulate osteoclasts directly or indirectly, which begin destruction of the alveolar bone. Thus, periodontitis sets in.
To add onto what tim has said(or break it down a bit i dunno) periodontal inflammation starts as inflammatory changes in the CT wall of the gingival sulcus-apical to the JE cells.Collagen fibres are damaged and the area becomes infiltrated with inflammatory cells. -JE becomes infiltrated with neutrophils -initial deepening of pocket by seperation of J from tooth -JE cells continue to migrate apically along root and seperate from epithelium inlateral wall of pocket. -Ct adjacent to epitherlium is densly infiltrated by chronic inflammatory cells(lymphocytes,macrophages & mastcells) and as tim explains the ability of the perio pocket can occur due to the bone resorbing ability.
Hope this helps and is correct... periodontal pockets constantly undergo cycles of inflmmation and repair however complete healing wont occur due to prescence of bactria.
Hi guys; Nicole.. here you have answered your previous scenario query... "periodontal pockets constantly undergo cycles of inflammation and repair however complete healing wont occur due to presence of bacteria".. so, if pockets are still present you still have disease.
Both of you are correct with your spread of inflammation... Do you know which gingival fibres are responsible for transmitting this inflammation to the underlying PDL?
I think it is the transepptal fibres coz the alveolar-periosteal blood vessels pierce transseptal fibres and inflammation then spreads down via blood to alveolar bone which then breaks down(pocket) and the transeptalfibrs form at a more apical level..
there is a diagram in the orange book near all the pathogenisis stuff if anyone wants to have a look. pg 68
5 comments:
Gingivitis is an inflammation of the gingival tissues. In early gingivitis there are increased levels of PMNs, T cells, immunoglobins and complement. There is only collagen loss in the infiltrated connective tissue. In established gingivitis, a pseudopocket is formed, with elevated GCF levels, plasma cells. There is further collagen loss and fibroblast damage.
At this stage there are many pro-inflammatory cytokines present, as well as PGE2, TNF.
After awhile, if the gram-negative bacteria in the plaque are present, and the host response is inadequate or inappropriate, periodontal destruction will begin. In this, there are elevated levels of macrophages which, as we know, can mediate the production of pro-inflammatory cytokines, oxygen radicals, and PGE2. These can stimulate osteoclasts directly or indirectly, which begin destruction of the alveolar bone. Thus, periodontitis sets in.
To add onto what tim has said(or break it down a bit i dunno)
periodontal inflammation starts as inflammatory changes in the CT wall of the gingival sulcus-apical to the JE cells.Collagen fibres are damaged and the area becomes infiltrated with inflammatory cells.
-JE becomes infiltrated with neutrophils
-initial deepening of pocket by seperation of J from tooth
-JE cells continue to migrate apically along root and seperate from epithelium inlateral wall of pocket.
-Ct adjacent to epitherlium is densly infiltrated by chronic inflammatory cells(lymphocytes,macrophages & mastcells) and as tim explains the ability of the perio pocket can occur due to the bone resorbing ability.
Hope this helps and is correct...
periodontal pockets constantly undergo cycles of inflmmation and repair however complete healing wont occur due to prescence of bactria.
Hi guys;
Nicole.. here you have answered your previous scenario query...
"periodontal pockets constantly undergo cycles of inflammation and repair however complete healing wont occur due to presence of bacteria"..
so, if pockets are still present you still have disease.
Both of you are correct with your spread of inflammation... Do you know which gingival fibres are responsible for transmitting this inflammation to the underlying PDL?
I think it is the transepptal fibres coz the alveolar-periosteal blood vessels pierce transseptal fibres and inflammation then spreads down via blood to alveolar bone which then breaks down(pocket) and the transeptalfibrs form at a more apical level..
there is a diagram in the orange book near all the pathogenisis stuff if anyone wants to have a look. pg 68
Well done Nicole!!!!!
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