Professional Documents
Culture Documents
Healthy
gingiva
Pathogenesis of Periodontitis
Normal
Current Thinking Tooth chrown gingival
sulcus
Gingiva is 2 to 3
millimeters
Massimo Costalonga D.M.D., Ph.D. deep
Root
Department of Developmental
and Surgical Sciences Periodontal
ligament
Alveolar bone
Advanced Background
periodontitis
Periodontal diseases:
Bleeding
Infection of the gingiva Infectious diseases that results in
Calculus chronic inflammation of the soft tissue
Gingival recession
Loss of bone surrounding the gingival pockets.
Tooth mobility
Halitosis (bad breath) Destroys the bone and soft tissue
connection between the gingiva and
the root of the tooth (Kornman 1987,
Disease that is not
reversible but ONLY Suzuki 1988)
controllable
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Massimo Costalonga DMD, PhD DENT5301
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Massimo Costalonga DMD, PhD DENT5301
Bacterial biofilm
16S RNA sequences separated
health and disease
Bacterial
challenge
Epithelium
Innate PMNs
Chemokines
immunity Cytokines
first
Kumar PS et al. 2005 Korman KS et al. Periodontology 2000 Vol. 14 1997, 33-53
Initial
Gingivitis How are these microbes
sensed or detected by our
Acute body?
inflammation
Talk with the person next to you
about this NOW
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Massimo Costalonga DMD, PhD DENT5301
PRRs
INNATE
Neutropenia = Low PMN counts cellular response
Monocytes/macrophages
Neutrophils
Natural Killer (NK)
Recognition of
Pathogen Associated
Molecular Patterns
(PAMPs) by Pattern
Recognition Receptors
(PRRs)
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Increase
Increase vascular
vascular
permeability
permeability
Increase
Increase smooth
smooth muscle
muscle
contraction
contraction
Increase
Increase smooth
smooth muscle
muscle
contraction
contraction
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Massimo Costalonga DMD, PhD DENT5301
Prostaglandins Lipoxins
Thromboxans Resolvins
Leukotrienes Protectins
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Massimo Costalonga DMD, PhD DENT5301
Interferon- Interleukin-4
(IFN) (IL-4)
Cell-mediated Antibody
immunity immunity
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Massimo Costalonga DMD, PhD DENT5301
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Massimo Costalonga DMD, PhD DENT5301
Destruction phase
Cytokine production most important IL- Induction of bone loss
1 but also TNF-, IL-6, IL-8, IL-12, IL-15 Osteoclast progenitors express the
and chemokines MCP-1 and RANTES receptor activator of NF-B (RANK)
Cytokine-induced alteration of the Activated T cells express the receptor
connective tissue metabolism activator of NF-B Ligand (RANKL)
Imbalance between collagenases and RANK / RANKL interaction + M-CSF
matrix metalloproteinases (MMPs) generates Tartarate-Resistant Acid
activity and collagen synthesis Phosphatase positive (TRAP+)
osteoclasts => BONE RESORPTION
IL-1 and IL-6 induce fibroblast and
osteoclast activation
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Massimo Costalonga DMD, PhD DENT5301
Potassium channel
blocker (kaliotoxin) T helper 2
Induced Protection and
Therapeutic Future B220 B cell T cell CD4
++ M-CSF
M-CSF
Potassium channel blocker
(Kaliotoxin) reduce the TRAP++
Osteoclast
expression of RANKL on T cells Bone
Destruction
Conclusion
Th1 type response IFN-mediated protects
from disease progression.
Th2 type response IL-4 and IL10-mediated
are inefficient at controlling microbial
biofilm.
Interference with RANK - RANKL
interaction of affects the degree of bone
loss
Cytokines and lipid mediators may mediate
systemic effects that increase the risk of
preterm birth and/or low birth weight