Oral Health and Systemic Disease Flashcards
biologically plausible mechanisms
oral bacteria, bacterial products, or local inflammation spreading to distant sites
bacteremia
presence of microbes in the blood stream due to tissue injury, medical or dental procedures
might be asymptomatic
higher risk for immunocompromised individuals
septicemia
bacteria multiplying in the blood stimulating a body wide response
septic shock
sepsis causing dangerously low blood pressure, therefore not enough blood reaching organs
focal infection
chronic oral infections by subgingival biofilms or periapical infections
bacteria or their products enter the gingiva
immune cells react by producing cytokines, can act locally
adverse immune response
cytokines produced in focal infection can enter the circulation
can cause other organs to have an adverse immune response
systemic diseases
examples of oral health affecting systemic health
atherosclerosis
rheumatoid arthritis
pregnancy
cancer
diabetes
respiratory disease
endocarditis
atherosclerosis
thickening and stiffening of arteries with accumulation of plaque in artery walls (fat, cholesterol, fibrosis, necrotic tissue)
“foam cells” - macrophage full of lipids
periodontitis and atherosclerosis associations
improving periodontal health
reduces system inflammation
reduces subclinical markers of atherosclerosis
decreases progression of carotid athersclerosis
P.gingivalis infection of rabbits
with high fat diet leads to local bone loss, but systemic inflammation and atherosclerotic lesions
P.gingivalis and atherosclerosis
-transcytosis or transmigration of bacteria
-recruits leukocytes
-leads to smooth muscle proliferation
-stimulates fat uptake by macrophages
-stimulates MMP release by neutrophils
-stimulates platelet aggregation
-TLR-2 dependent
P.gingivalis and rheumatoid arthritis
autoimmune disease
inflammation and thickening of joint capsule, degradation of cartilage and bone loss
deposition of immune complexes on the joint membrane (Type 3 hypersensitivity)
rheumatoid factor
an autoantibody (IgM) that binds to the Fc region of IgG
anti-citrullinated proteins autoantibodies
citrulline
an amino acid not encoded by one of the 64 codons
enzymatically arginine deiminases or peptylarginine deiminase (PAD)
p.gingivalis and rheumatoid arthritis requires
molecular mimicry
the citrullinated host proteins must resemble something citrullinated by PAD
p.gingivalis and rheumatoid arthritis mechanism
arginine is converted to citrulline by p.gingivalis PAD
citrullination changes antigenicity of peptide (B cell can recognize)
citrullinated proteins are presented in HLA class II to T helper cells
antibodies against the citrullinated proteins (ACPAs) are produced
humans also have PAD which also converts arginine to citrulline, the citrullinated host proteins are recognized by ACPAs
complex may deposit in the joints and activate complements, plus other immune response, lead to local inflammation in the joint and may lead to rheumatoid arthritis
fusobacterium nucleatum
Gram-negative anaerobic bacterium
in supra-gingival and sub-gingival dental plaques
able to interact with other species of bacteria, promoting dental plaque development
“bridging” bacterium
potential periodontal pathogen
low-birth weight, pre-term birth, miscarriage
can cross placenta
associated with colorectal cancer
F. nucleatum and cancer
adhesin FadA
E-cadherin-FadA interaction to bind endothelial cells
activation of oncogenic and inflammatory genes
F. nucleatum and pregnancy
adhesin FadA
E-cadherin-FadA interaction to bind endothelial cells
crosses the endothelium and colonize the fetal placental compartment
TLR4-dependent inflammatory responses
p. gingivalis and cancer
associated with oral squamous cell carcinoma, orodigestive cancer, pancreatic cancer
immune evasion strategies can overlap with oncogenic signaling pathways (gingipains)
oral health and diabetes
increase risk of periodontitis severity
increase glucose in saliva
can reduce salivary flow
affects immune cell functions: increase inflammation in periodontium, increased production TNFa, reduced effectiveness in bacterial killing
functions of periodontal ligament cells, osteoblasts, osteocytes (reduce bone formation)
