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Pathogenesis..
Periodontal diseases:
Bacterial Plaque
Host response
Immune system
Inflammation
Clinical signs
Pathogenesis..
Periodontal diseases: Bacterial Plaque
Host tissues
Host Response
Pathogenesis..
Periodontal diseases: Bacterial Plaque
Host tissues
Protective or Destructive?
Host Response
So..
The presence of periodontal pathogens alone is
insufficient to cause the tissue destruction seen in periodontitis. It is the bodys response to the periodontal pathogens that is the cause of nearly all the destruction seen in periodontitis.
Bacterial Characteristics
Bacterial invasion factorsallow
bacterium to actively penetrate the
Bacterial Products
Exotoxinsharmful proteins (potent
toxin) released from the bacterial cell
Enzymesproteins that catalyze chemical reactions that are harmful to the bodys cells
Bacterial Colonization
Coaggregation of Bacteria
Coaggregationthe cell-to-cell adherence of one oral bacterium to another.
Coaggregation is NOT random, each bacterial strain only has a limited set of bacteria to which they are able to adhere.
Coaggregation of Bacteria
Early Intermediate Late
Early Colonizers
The first bacteria to colonize the tooth
surface are nonpathogenic. Periodontal pathogens are UNABLE to colonize the biofilm alone.
Tooth/ or hard tissue NonPathogenic Pathogenic
Streptococcus sanguis
Intermediate Coaggregation
Bacteria begin to multiply.
Gram-Negative Organisms
Gram-negative bacteria join: Fusobacterium nucleatum Prevotella intermedia
Gram-Negative Organisms
Gram-negative bacteria colonize Porphyromonas gingivalis Capnocytophaga gingivalis
Biochemical Mediators
Biochemical Mediators
Released by the immune cells to activate the inflammatory response.
Cytokines
Cell signalling protein molecules Powerful mediators produced by immune cells Influence the behavior of other cells Signal to the immune system to send more phagocytes to site of infection
Cytokines (cont.)
Produced by many different cellsPMNs, macrophages, B lymphocytes, epithelial cells, gingival fibroblasts, and osteoblasts Produced in response to tissue injury Cytokines important in periodontal disease include IL-1, IL-6, IL-8, and TNF-alpha.
Functions of Cytokines
Recruit cells (PMNs and macrophages) to infection site
Increase vascular permeability that increases movement of immune cells into the tissues Can initiate tissue destruction and bone loss in chronic infections, such as periodontal disease
Prostaglandins
Potent inflammatory mediators Series of prostaglandinsD, E, F, G, H, I Most cells can produce prostaglandins (arachidonic acid in the cell membrane)
Functions of Prostaglandins
Increase permeability and dilatation of blood vessels to promote increased movement of immune cells and complement to the infection site
Trigger osteoclastsbone-consuming
cellsto destroy the alveolar bone
Functions of Prostaglandins
Promote the overproduction of destructive MMP enzymes Prostaglandins of the E series (PGE) initiate most of the alveolar bone destruction in periodontitis.
Initial
gingival margin.
Bacteria initiate host response. PMNs pass from bloodstream into the gingival connective tissue.
Early
Bacteria penetrate into the connective tissue. PMNs release cytokines causing more localized destruction of the connective tissue. Macrophages release cytokines, PGE2, and
MMPs.
Established
chemicalscytokines, PGE2,
and MMPs.
Advanced
Cytokines, PGE2, and MMPs destroy the connective tissue and bone.
Macrophages produce cytokines, PGE2, and MMPs. This will stimulate fibroblasts to secrete PGE2 and MMP. Destruction of the connective tissue. PGE2 stimulates osteoclasts to resorb the alveolar bone.