periodontal destruction Flashcards
destructive pathways
1) host response is associated with bone and attachment loss triggered by bacteria
gingival health
1) few inflammatory cells present with no proliferation of the junctional epithelium
initial lesion
1) preclinical gingivitis
2) 2-4 days of plaque accumulation
3) loss of perivascular collage
4) neutrophil migration
5) increased GCF
early lesion
1) early clinical gingivitis
2) 4-7 days plaque
3) lymphocyte infiltration
4) loss of collagen up to 70%
5) proliferation J.E.
6) few plasma cells
established lesion
1) chronic gingivitis
2) 2-3 weeks plaque
3) plasma cells predominate
4) continued loss of collagen
5) no bone loss
6) apical migration of JE
7) pocket formation
advanced lesion
1) periodontitis
2) plasma cells predominant
3) fibrosis
4) pocket formation
5) continued apical migration of JE
6 )bone loss
principles of pathogenesis
1) bacterial plaque is essential => host response => connective tissue and bone loss => clinical signs of disease
quality and quantity of plaque
1) does not explain disease severity by themselves
2) host factors influenced by genetic and environmental
smoking
1) huge risk factor
2) odds ratio for advanced periodontal disease
- former smoker - 2
- current smoker - 3
3) masks inflammation
twin studies
1) more than 40% of clinical signs of disease were due to genetics
IL-1 genotype
1) genotype positive people will produce way more of it
2) activates osteoclasts
host response
1) non specific
2) specific
complement
1) first line of defense
2) resolution of acute inflammation
neutrophils
1) second line of defense
2) resolution of acute inflammation
monocyte macrophage
1) present bacterial antigens to Helper T
2) resolution of chronic inflammation
lymphocytes
1) Ab, Ab+, and CMI control
2)if not, could be systemic infection
periodontal inflammation
1) localized protective response which serves to destroy, dilute, or wall off both the agent (microbes) and the injured tissue
2) redness, swelling ,heat and pain
cytokines
1) soluble messenger proteins
2) inflammation, immune growth, differentiation processes
3) can be pro inflammatory or anti inflammatory
MMP
1) remodeling and degradation of the ECM components in the periodontium
2) pro-inflammatory
prostaglandin E2
1) proinflammatory mediators that cause bone destruction
2) arachidonic acid derivative
proinflammatory mediators
1) IL-1, IL-6, IL-8, TNF-alpha
2) PGE2
3) MMPs
4) leukotrienes
IL-1
`) simulates osteoclasts
2) secreted by macrophages, B cells, others
3) T cell activation
4) promote B cell maturation
5) chemotaxis
TNF alpha and beta
1) alpha by macrophages and mast cells
2) beta by helper T cells
3) activation of osteoclasts
4) phagocytosis and chemotaxis
IL-6
1) T cells, macrophages, others
2) T cell activation and plasma cell production
3) role in bone resorption
antiimflammatory mediators
1) IL-4, IL-10, IL-1ra
2) tissue inhibitors of MMPs
3) lipoxins
innate immune response
1) non specific
2) complement
3) toll like receptor
4) neutrophil
5) macrophages
—
1) recognize bacterial products
2) recruit inflammatory cells
3) proinflammatory mediators
4) activate osteoclassts
5) bone, ECM, and collagen destruction
serum complement
1) >30 soluble serum proteins and cell receptors
2) enables endothelium and leukocytes to recognize foreign substances for which they lack a receptor
3) C3a and C5a
4) role in transendothelial migration
—
1) direct (classical) by immune complexes IgG and IgM
2) alternate pathway
=> opsonization, cell lysis, chemotaxis and histamine release
toll like receptors
1) pattern recognition receptor
2) mainly cells in first line of defense
- neutrophiles, macrophages
3) recognize endotoxins (LPS)
non specific cellular response
1) neutrophils
2) monocyte / macrophages
transendothelial migration
1) cells gently rolling allow bloodstream
2) complement activated, C3a and C5a => activate resident leukocytes like mast cells
3) endothelium makes p-selectin, e-selectin bind carbs on surface of leukocyte
- more rolling!
4) TNF from mast cells stimulated endothelium to release IL-8
- bind CXCR2 receptor on leukocytes
- L-selectin is shed
5) LFA is expressed and binds to cellular adhesion molecules ICAM2 on endothelium
- no more rolling
6) CD31 on leukocyte and on the endothelium
- lines it up with junction on epithelial cells
- unzips it
7) gets into the tissues with minimal leakage
once in the tissue
1) leukocyte follows the chemical gradient to the bacteria
PMN
1) differentiate in bone marrow
2) rapid response
monocyte
1) differentiate in local tissue
2) present antigen to T cell
specific host response
1) activated when first line of defense in insufficient
2) specialized functions regulated by lymphocytes
1) humoral
2) cellular
activating specific host response
1) macrophage IL-1 and IL-6 for activating helper T cells
2) tells B cells to differentiate into plasma cells
humoral immunity
1) bone marrow
2) b lymphocytes
3) memory cells, plasma cells, cytokines
IgA and IgM
1) immune complexes
2) opsonins for neutrophils and macrophages to phagocytosis
–
1) activate complement
IgA
1) regulate bacterial colonization in mouth
IgE
1) mast cells
2) degranulation and histamine
vascular response
1) redness, heat, swelling, pain
cellular immune response
1) bone marrow => thymus => t lymphocytes
2) memory cells, cytokines, cytotoxic and T helper cells
Mast cell
Resident leukocyte that releases histamine, TNF, others
- rule in vascular response
