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Perio I Supplemental Cards > Systemic Perio Disease > Flashcards

Systemic Perio Disease Flashcards

1
Q

from a historical perspective, there is a long-standing awareness of certain links between oral health and ___, and of systemic effects on ___

A
  • systemic health
  • oral tissues
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2
Q

special considerations are needed for patients with ____

A

systemic conditions

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3
Q

during disease (periodontitis), there is a high level of what 5 pro-inflammatory molecules?

A
  • IL-1beta
  • TNF-alpha
  • INF-gamma
  • PGE2
  • MMPs
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4
Q

during disease (periodontitis), there is a low level of what 5 pro-inflammatory molecules?

A
  • IL-4
  • IL-10
  • TGF-beta
  • IL-1ra
  • TIMPs
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5
Q

during health (no periodontitis), there is a low level of what pro-inflammatory molecules?

A
  • IL-1beta
  • TNF-alpha
  • INF-gamma
  • PGE2
  • MMPs
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6
Q

during health (no periodontitis), there is a high level of what pro-inflammatory molecules?

A
  • IL-4
  • IL-10
  • TGF-beta
  • IL-1ra
  • TIMPs
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7
Q

compelling evidence suggests periodontitis may be related to the risk for what 4 diseases?

A
  1. cardiovascular disease
  2. preterm low-birth weight infants
  3. diabetes
  4. respiratory disease

possibly others

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8
Q

name 5 conditions that can have risk factors associated with periodontitis

A
  • osteoporosis
  • menopause
  • pregnancy
  • smoking/ethanol use
  • HIV
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9
Q

from a systemic standpoint, what are 5 implications of periodontics for practice?

A
  • emphasize the importance of oral health to overall well-being
  • reducing inflammatory burden
  • recognize systemic signs and symptoms and be prepared to refer patients to a physician
  • clearer links between oral health and systemic health may necessitate practice adjustments
  • all patients should be screened for periodontal disease
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10
Q

clearer links between oral health and systemic health may necessitate practice adjustments for what 4 types of patients?

A
  1. people with diabetes
  2. pregnant women
  3. patients at risk for cardiovascular disease
  4. elderly patients
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11
Q

can SBE prophylaxis prevent infective endocarditis?

A
  • only in an extremely small number of cases
  • it is still recommended for patients with underlying conditions associated with highest risk for infective endocarditis
  • recommendations based on “prevention of infective endocarditis - guidelines from the American Heart Association 2007”
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12
Q

“prevention of infective endocarditis - guidelines of the american heart association - 2007” recommends that patients at high risk for infective endocarditis who are receiving any of what 3 types of care should also receive SBE prophylaxis?

A
  • manipulation of gingival tissues
  • manipulation of the periapical region
  • perforation of the oral mucosa
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13
Q

according to “prevention of infective endocarditis: guidelines from the american heart association - 2007”, antibiotic prophylaxis with dental procedures is recommended only for patients with cardiac conditions associated with the highest risk of what 2 adverse outcomes from endocarditis?

A
  • prosthetic cardiac valce
  • previous endocarditis
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14
Q

according to the “prevention of infective endocarditis: guidelines from the american heart association - 2007”, patients with congenital heart disease from which 4 categories should receive antibiotic prophylaxis?

A
  • Unrepaired cyanotic congenital heart disease, including those with palliative shunts and conduits
  • Completely repaired congenital heart disease with prosthetic material or device, whether placed by surgery or catheter intervention, during the first six months after the procedure
  • Repaired congenital heart disease with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
  • Cardiac transplantation recipients with cardiac valvular disease
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15
Q

how many people in the US have diabetes?

how many diagnosed, undiagnosed, and pre-diabetes cases are there in the US?

how many deaths were associated with diabetes in 2007 in the US?

diabetes is the ___ leading cause of death in the US

A
  • 25.8 million people - 8.3% of the US population
  • diagnosed: 18.8 million people
  • undiagnosed: 7 million people
  • pre-diabetes: 57 million people
  • 231,404 deaths in 2007
  • 7th leading cause of death
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16
Q

how many people in the following categories have diabetes?

age 20 years or older
age 65 years or older
men age 20 or older
women age 20 or older
non-hispanic whites
non-hispanic blacks

A
  • age 20 years or older: 25.6 million, or 11.3%
  • age 65 years or older: 10.9 million, or 26.9%
  • men: 13 million, or 11.8%
  • women: 12.6 million, or 10.8%
  • non-hispanic whites: 15.7 million, or 10.2%
  • non-hispanic blacks: 4.9 million, or 18.7%
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17
Q

what are 3 main characteristics of diabetes?

A
  • fasting blood glucose levels >126 mg/dL after overnight fast
  • 2-hr blood glucose level >200 mg/dL after a 2-hr oral glucose tolerance test (OGTT)
  • an HbA1c level >6.5%
  • *the first 2 are 2 of 3 methods used to diagnose diabetes*
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18
Q

what are the 4 main classifications of diabetes, and what percentage of the population has each type?

A
  • type 1 (IDDM); 5-10%
  • type 2 (NIDDM); 90-95%
  • gestational diabetes (due to pregnancy); 3-5% of all preg.
  • secondary diabetes; 1-2%
  • impaired glucose tolerance/impaired fasting glucose
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19
Q

describe causes of secondary diabetes

A
  • recurrent pancreatitis, pancreatectomy endocrine disorders
  • steroid drug therapy/misuse
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20
Q

describe diabetes

A
  • a metabolic disorder in which the body does not produce or use insulin properly
  • affects approxmiately 7% of people int he united states - almost 21 million people
  • 6th* leading cause of death among americans
    *earlier slide claims that it is the 7th leading cause
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21
Q

describe type 1 diabetes

A
  • insulin is not created at all
  • accounts for about 5-10% of diabetes cases
  • requires daily insulin supplementation
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22
Q

describe type 2 diabetes

A
  • insulin is produced, but use ineffectively
  • accounts for 90-95% of diabetes cases
  • occurs most often in people who are overweight
  • may or may not require modificaiton
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23
Q

describe gestational diabetes

A
  • glucose intolerance that is diagnosed during pregnancy
  • requires treatment to normalize maternal blood glucose levels to avoid complications in the infant
  • frequency varies among the female population
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24
Q

gestational diabetes is more frequent among what members of the female population?

A
  • african americans, hispanic/latino americans, and american indians
  • obese women and women with family history during pregnancy
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25
Q

describe how gestational diabetes during pregnancy affects women after pregnancy

A
  • 5-10% of women have type 2 diabetes
  • 20-50% chance of developing diabetes in the following 5-10 years
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26
Q

what are 3 main disorders related to diabetes?

A
  • insulin resistance
  • production of AGEs (advanced glycosylation end products)
  • metabolic syndrome
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27
Q

describe insulin resistance

A
  • common symptom of type 2 diabetes
  • insufficient insulin produced by the pancreas, OR
  • improper insuling functioning at the cellular level
  • sugar is locked out of the cells and builds up in the blood
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28
Q

describe metabolic syndrome

A
  • a set of “abnormalities” involving waist size, weight, blood pressure, lipid levels, and blood glucose levels
  • affects about 47 million people in the US
  • associated with increased risk for developing diabetes and cardiovascular disease as well as increased mortality from cardiovascular disease and all causes
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29
Q

what are the 6 classic complications of diabetes?

A
  • retinopathy
  • nephropathy
  • neuropathy
  • cardiovascular disease
  • altered wound healing
  • periodontal disease
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30
Q

relative to diabetes, patients presenting for dental care will fall into one of what 4 categories?

A
  • diagnosed and controlled
  • diagnosed and uncontrolled
  • family history: diagnosed/undiagnosed
  • undiagnosed
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31
Q

what are 9 signs/symptoms of the undiagnosed or uncontrolled diabetic?

A
  • excessive thirst (polydipsia)
  • excessive urination (polyuria)
  • unexplained weight loss
  • vision changes
  • weakness, malaise
  • irritability
  • nausea
  • dry mouth
  • ketoacidosis (sweet-smelling, fruity breath from acetone)
  • extreme hunger
  • frequent infection/impaired wound healing
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32
Q

what are 2 types of glucose monitoring?

A
  • glucometer
  • glycosylated hemoglobin
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33
Q

describe glucometers

A
  • widespread use
  • use depends on treatment regimen/compliance
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34
Q

describe glycosylated hemoglobin

A

hemoglobin + glucose = glycosylated hemoglobin

  • HbA1 (less common)
  • HbA1c (home/office test available)
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35
Q

what are the 3 diagnostic criteria used to diagnose diabetes?

A
  1. casual (random) plasma glucose: >200 mg/dL without regard to time since last meal; signs/symptoms of diabetes present
  2. fasting plasma glucose: >126 mg/dL; no caloric intake for at least 8 hours
  3. 2-hr post-prandial glucose: >200 mg/dL during an oral glucose tolerance test 75 grams (not recommended for routine clinical use)

only one of these 3 criteria is required for diagnosis; whichever method is used must be confirmed on a subsequent day

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36
Q

what are normal values for glycosylated hemoglobin assay control (HbA1 and HbA1c) tests?

A
  • HbA1: 5.8-8.4%
  • HbA1c: 4.5-6.7%
  • normal values differ between labs; important to know lab’s reference standard
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37
Q

glycosylated hemoglobin (HbA1c) levels reflect glucose levels in the blood over the preceding 30-90 days. describe the common %total hemoglobin and it’s clinical interpretation

A
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38
Q

describe how HbA1c (%) levels correlate to average plasma glucose levels

A
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39
Q

describe how advanced glycation end products (AGEs) effect connective tissue during the repair process

A
  • Structural changes by forming cross-links in tissue fibers
  • Reactions with cellular receptors of advanced glycation end products (RAGEs)
  • Increased production of inflammatory molecules
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40
Q

T or F:
smoking impacts the repair process

A

true

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41
Q

describe advanced glycation end-products (AGEs)

A
  • Non-enzymatic addition of hexoses to proteins
  • A.G.E.s can interfere with the proper functioning of the proteins to which they are attached
  • HbA1c -measures levels of glycated hemoglobin eg serum glucose over preceding 2-3 months
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42
Q

advanced glycation end-products (AGEs) result in what 3 things?

A
  • Collagen accumulation in periodontal capillary membranes - membrane thickening
  • Stimulation of smooth muscle increases thickness of vessels
  • Binding of LDL to AGE-modified collagen
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43
Q

AGEs result in binding of LDL to AGE-modified collaged. what can this cause?

A
  • artheroma formation
  • narrowing of vessel lumen
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44
Q

AGEs cause alterations in collagen turnover, which can effect wound healing in what 3 ways?

A
  • Increased collagenase (MMP) production: Degrades newly formed collagen
  • Decreased solubility: Accumulation of AGE modified collagen
  • Net result in decrease turnover which leads to increased damage and less wound healing
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45
Q

in what 3 ways do AGEs impair PMN function?

A
  • leukocyte adherence
  • chemotaxis
  • phagocytosis
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46
Q

T or F:

AGEs do not cause significant defects in first line of defense

A

false:

they cause significant defects in first line of defense

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47
Q

monocytes, macrophages, and endothelial cells posses high affinity receptors for AGEs (called RAGEs). the binding of monocytes/macrophages to RAGEs results in hyper responsive release of what?

A
  • IL-6
  • TNF-alpha
  • PGE2
  • increase secretion IL-1beta
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48
Q

in what 3 ways to AGEs effect endothelial cells?

A
  • procoagulatory changes leading to focal thrombosis and vasoconstriction
  • hyperpermeable
  • hyperexpression of adhesion molecules
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49
Q

does diabetes effect periodontal health?

A
  • Most studies suggest a greater prevalence, severity, extent and progression of periodontal disease in the diabetic. (Type 1 and 2)
  • 37/41 cross sectional (III)
  • 7/7 cohort (II)
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50
Q

describe the findings of cross-sectional studies on the effects of glycemic control on periodontitis

A
  • 19/34 more frequent or severe disease in patients with poor glycemic control
  • 15/34 report no differences
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51
Q

what were the effects of glycemic control on periodontitis found by studies conducted before and after 1990?

A
  • before 1990: 6/16 more frequent periodontal disease/poor control
  • after 1990: 13/18 more frequent periodontal disease/poor control
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52
Q

describe how effects of glycemic control on periodontitis are difficult to interpret in studies

A
  • differences in populations studied (age, race, etc.)
  • differences in periodontal disease measurements (inflammation, probing, loss of attachment, radiographs, etc.)
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53
Q

describe the effects of periodontal treatment and glycemic control

A
  • 5/12 evidence to support that periodontal treatment does modify glycemic control
  • 7/12 equivocal or no change
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54
Q

describe how the different modes of periodontal treatment/therapy are related to glycemic control

A
  • mechanical only: no change in glycemic control
  • mechanical plus systemic antibiotics: improved glycemic control
55
Q

describe 3 main conclusions found from studies that correlated the effects of glycemic control on periodontitis

A
  • evidence clearly supports a relationship between diabetes and periodontal disease
  • the relationship is most likely bidirectional
  • additional studies needed to establish this relationship
    • treatment of periodontal disease contributes to glycemic control
    • reduces complications of diabetes
56
Q

describe obesity

A
  • affects up to 30% of the US population
  • linked to a number of serious health concerns, including diabetes an dperiodontal disease (the 3-way street)
57
Q

describe the 3-way street (interaction between obesity, diabetes, and periodontal disease)

A
  • Fat is an inflammatory tissue, which releases TNFa, C-reactive protein, and other cytokines
  • Cytokines can lead to insulin resistance and type 2 diabetes
  • Obesity is a risk factor for both type 2 diabetes and periodontal infection
  • Diabetes heightens risk for periodontal disease
  • Inflammation triggered by the proinflammatory cytokines manufactured by fat tissue and produced by gingival infection exacerbates both conditions
58
Q

what are 2 main reasons there is a higher prevalence of tooth loss in people with diabetes?

A
  • elevated inflammatory response
  • decreased ability to fight infection
59
Q

treatment of periodontal disease reduces the need for ___

A

insulin

60
Q

___ and other cytokines may interfere with the action of insulin and glycemic control

A
  • TNF-alpha
    • for example, glycated hemoglobin may be affected
61
Q

what are 3 oral signs of diabetes?

A
  • foamy saliva
  • unusually dry and irritated tissue
  • severe periodontal inflammation
62
Q

what are the target glucose levels in type 2 diabetes?

A
  • fasting plasma glucose 90-130 mg/dL
  • postprandial plasma glucose <170 mg/dL
63
Q

from a periodontal perspective, what are 4 main ways to treat patients with diabetes?

A
  • manage soft tissue inflammation
  • more frequent recall schedule (3-4 months)
  • proper home care
  • monitoring blood glucose levels
64
Q

according to the 2000 surgeon general’s report on oral health in america, almost ___ of people with diabetes have severe periodontal disease. interaction between periodontal disease and diabetes is still being investigated.

A

1/3

65
Q

periodontal disease can cause vascular lesions as a result of bacteria and bacterial products. describe the 2 effects of bacteria and bacterial products

A
  • direct effect on monocytes/macrophages
    • release IL-1, IL-6, TNF-alpha
    • result in vascular lesion
  • indirect effect
    • stimulate liver
    • release CRP (C-reactive protein), fibrinogen, lipid abnormalities, coagulation factors
    • result in vascular lesion
66
Q

what are 2 well established risk factors for cardiovascular disease?

A
  • tobacco smoking
  • high LDL
67
Q

evidence has identified ___ as an important risk factor for myocardial infarction, and causes a ___-fold increase in risk

A
  • CRP
  • 2-5
68
Q

in relation to cardiovascular disease, NHANES III data found that periodontitis increased systemic ___ and ___ when adjusted for other parameters

A
  • CRP
  • plasma fibrinogen
  • other data showed that CRP levels increase in periodontitis vs. healthy patients, and one year perio treatment showed a reduction of CRP
69
Q

atherosclerotic plaques pathogenesis includes which 5 characteristics?

A
  • endothelial damage/dysfunction
  • lipid deposition and oxidation in the subendothelial space
  • macrophage/PMN chemotaxis
  • smooth muscle proliferation
  • plaque rupture
70
Q

inflammation within atherosclerotic plaque causes what?

A
  • fibrous cap thinning
  • plaque rupture
  • thrombosis
71
Q

breakdown of atherosclerotic plaque leads to what?

A
  • myocardial infarction
  • unstable angina
  • stroke
  • TIAs
72
Q

what is MCP1?

A
  • monocyte chemotactic protein-1
  • member of the small inducible gene (SIG) family
  • role in recruitment of monocytes to sites of injury and infection
73
Q

where is the gene for MCP1 found?

A

chromosome 17 in region 17q11.2-q12

…yeah

74
Q

describe characteristics of MCP1

A
  • found in the joints of people with rheumatoid arthritis
  • elevated in urine as a sign of kidney inflammation
  • associated with diabetes
75
Q

the remnants of what 2 lipoproteins are proinflammatory?

A

chylomicrons and VLDL

76
Q

what are 3 pieces of evidence for a role of periodontitis in atherosclerosis

A
  • periodontal pathogens have been identified in human carotid atheromas
  • NF-kappaB (nuclear factor-kappa B)
  • production of cross reacting antibodies between periodontal bacteria and HSP of the heart
77
Q

describe characteristics of NF-kappaB

A
  • stimulation of cells with LPS, TNFalpha and IL-1beta induces formation of NF-kappaB
  • stimulates macrophage activation and smooth muscle cell proliferation
  • constant stimulation of cells with these inflammatory mediators perpetuates the cycle
78
Q

describe the treatment of periodontal disease as it relates to cardiovascular disease

A
  • SCRP and subgingival doxcycline
    • reduced CRP and fibrinogen to normal levels
  • PMT aimed at reducing P. gingivalis
    • maintains CRP and fibrinogen at normal values with time
  • SCRP and subgingival minocycline
    • reduced CRP and TNF alpha in patients with increased risk for CVD
79
Q

what do in vitro and in vivo animal studies suggest about periodontal disease and heart disease?

A

periodontal disease and cardiovascular disease may be due to the potential for oral bacteria (s. sanguis and p. gingivalis) to induce platelet aggregation

80
Q

animal studies of the link between periodontal disease and heart disease have shown that platelets aggregate in response to s. sanguis and p. gingivalis as a result of mistaken identity. explain.

A

a protein structure on the surface of common strains mimic the platelet-interactive regions of collagen molecules

81
Q

describe evidence for a role of periodontitis in myocardial infarction from case controlled/ cross sectional studies

A

show a significant association between poor dental health and CHD

82
Q

describe evidence for a role of periodontitis in myocardial infarction from longitudinal studies

A
  • demonstrate that poor oral health precedes cardiovascular events
  • dose relationship between levels of bone loss and the cumulative incidence of angina and MI
83
Q

T or F:

studies on subgingival plaque demonstrate an association with MI

A

true

84
Q

is periodontitis an independent risk factor for cardiovascular disease or stroke?

A

no, but consistent findings point to an association between periodontitis and an increased risk for CVD

85
Q

do methods to establish periodontal disease vary?

A

yes, widely

86
Q

further studies of the association between periodontitis and CVD should include what?

A
  • determine whether period dx alone or in presence of other oral infection increases cardio or cerebrovascular disease
  • elucidate underlying pathologic mechanisms
  • clarify confounding effects of sex, age, smoking, and race/ethnicity
87
Q

describe the clinical association between periodontitis and atherosclerosis

A
  • supported by some studies
  • not supported by others
  • most recent study lends direct support for the hypothesis
88
Q

describe the evidence for an association of periodontitis and stroke for men under 50

A
  • 25% of the patients who had a stroke had significant dental disease
  • 2.5% in the control group without CVA
89
Q

describe evidence suggested by NHANES I data analysis for an association of periodontitis and stroke

A
  • periodontal disease is a significant risk factor for non-hemorrhagic stroke but not for hemorrhagic stroke
  • seen in white and black men and women
  • physician health study showed similar findings
90
Q

what are the two major categories of stroke? what are their relationships to periodontal disease?

A
  • hemorrhagic
    • caused by bleeding into the brain
    • not associated with periodontal disease
  • nonhemorrhagic, or ischemic
    • caused by blockage of a blood vessel supplying the brain
    • associated with periodontal disease
91
Q

describe how to treat a patient with CVD

A
  • conduct medical history and physical exam
  • identify physical signs and symptoms of cardiac dysfunction - craniofacial pain
  • evaluate vital signs
  • seek medical consultation when indicated
  • know concomitant medications
  • be aware of conditions requiring antibiotic prophylaxis
92
Q

describe female sex hormones

A
  • estrogen and progesterone can be used by some bacteroides species (G-anaerobes) as substitutes for menadione (vit K), one of their important growth factors
  • use of contraceptives also use gestational hormones that can also lead to increased gingival inflammation
93
Q

describe the relationship between pregnancy and gingivitis

A
  • increase in gingivitis independent of plaque accumulation
  • increase mirrors increasing estrogen and progesterone levels in months 4-9
  • no attachment loss noted and the condition is self-limiting and reversible
  • p. intermedia and other bacteroides species can use estrogen and progesterone as a vit K substitute needed for growth
  • connective tissue breakdown may be enhanced by plasminogen activator activating the fibrinolytic system
94
Q

leukocyte adhesion deficiency (LAD) is due to deficiency in cells surface integrins. describe this

A
  • leukocytes cannot adhere to wall of endothelium at sites of infection (no diapedesis or migration from capillaries into soft tissues)
  • no migration to site of infection
  • generally results in early death if untreated with bone marrow transplant
  • loss of primary and permanent teeth
95
Q

describe chediak-higashi

A

azurophilic inclusions in cytoplasm hinders migration and phagocytosis of microbes

  • platelet abnormalities lead to bleeding abnormalities
  • average lifespan is 6 years
  • severe gingivitis, early onset periodontitis, lesions of tongue and buccal mucosa
  • premature loss of primary and permanent teeth
96
Q

describe cyclic neutropenia

A
  • characterized by a cyclical decrease in neutrophils on a roughly 21 day cycle and a 3-10 day period of severe neutropenia
    • can have 3-6 days of feber, malaise, mood swings, and oral ulcerations
    • periodontitis may progress faster during periods of neutrophil depression
    • tooth can result from periodontitis (???)
97
Q

describe congenital neutropenia

A
  • characterized by a low absolute neutrophil count
  • results from arrested neutrophil hematoporesis
  • severe bacterial infections
  • periodontitis with bone loss in most cases
98
Q

describe papillon-lefevre syndrome

A
  • results from mutation in cathepsin C gene on chromosome 11
  • decreased chemotaxis, phagocytosis, and intracellular bacterial killing
  • rapid generalized destruction of periodontal attachment
  • premature primary and permanent tooth loss
99
Q

describe down syndrome

A
  • neutrophils tend to be normal
  • chemotaxis, phagocytosis, and intracellular killing may be reduced
  • collagenase from salivary and crevicular fluid neutrophils may be increased
  • more periodontal disease noted than suggested by the level of local factors
100
Q

describe leukemias

A
  • sometimes the first sign of the disease is seen in the oral cavity
  • mucosal ulcerations and gingival enlargement are among the most common oral signs of the acute monocytic form of the disease
101
Q

describe wegener’s granulomatosis (aka strawberry gingivitis)

A
  • granulomatous necrotizing vasculitis of small vessels of the upper and lower respiratory tract
  • characterized by hyperplastic gingivitis
  • can result in tooth mobility and tooth loss
102
Q

what is a genotype?

A

genetic constitution of the cell; DNA sequence

103
Q

describe phenotype

A
  • any observable characteristic or trait of an organism such as morphology, development, biochemical or physical properties, or behavior
  • phenotype is the interplay between the inherited genotype, transmitted epigenetic factors, and non-hereditary environmental variation
104
Q

describe transcription-translation

A
  • DNA is transcribed by RNAP to create mRNA
  • which sections of the DNA that is transcribed is controlled by the promoter and ending codons
  • mRNA leaves the nucleus to interact with rRNA and tRNA to form polypeptide chains (proteins)
105
Q

mutations and gene therapy:

describe alterations in the DNA base that can result in changes in protein structure and function

A
  • insertions
  • deletions
  • polymorphisms
  • etc.
106
Q

mutations and gene therapy:

name 3 diseases that result from single gene defects

A
  • cystic fibrosis
  • sickle cell anemia
  • papillon-lefevre syndrome (mutated cathepsin C receptors)
107
Q

what are 4 types of gene therapy?

A
  • gene insertion therapy
  • liposomes
  • antisense
  • methylation
  • single gene diseases may be amenable to such treatment
108
Q

most diseases are multifactorial with a genetic component as the basis. describe this.

A
  • gene variations or polymorphisms (ex. IL-1 gene)
  • these genetic risk factors may be associated with various loci (multi-gene diseases)
  • genetic insufficiency does not lead to clinical manifestations of disease but over time, the patient becomes more susceptible to chronic periodontitis
109
Q

describe 6 defects and polymorphisms with risk for periodontitis

A
  • Fc receptors (FCgammaRII on PMNs)
  • IgG2 level
  • Il-1 gene (+) polymorphisms
  • COX-1 (+) gene: elevated PGE2 production
  • monocyte (+) phenotype: inflammation/ wound healing
  • receptor polymorphisms for:
    • IL-4, IL-10, TNFalpha, FMLP, Vit D3, cathepsin-C
110
Q

what is epigenetics?

A

meiotic and mitotic inherited changes in gene expression not encoded into the DNA sequence itself

111
Q

describe chromatin

A
  • DNA does not exist in a naked state
  • DNA is bound to histone proteins in individual units referred to as nucleosomes
  • these protein complexes can pack and unpack the chromasomal DNA from accessible relaxed DNA to inaccessible condensed DNA
112
Q

describe DNA methylation by DNA methyl-transferases

A
  • bacteria use DNA methylation as a main mechanism for turning on and off transcription
  • widespread methylation can silence gene transcription
113
Q

describe histone modification

A
  • histones positively charged and bind tightly to DNA
  • histone acetylases and histone deacetylases required
  • methylation and phosphorylation can also occur
  • charge changes results in more relaxed configuration favoring gene expression
  • the insulin gene in insulin-producing pancreatic cells display histone modificaitons typical of active genes
    • x-chromosome silencing
    • allelic silencing
114
Q

describe the role of folate in epigenetics

A
  • folate deficiency results in open tube defects
  • folate is an essential factor in conversion of methionine to S-adenosylmethione, the methyl group donor in DNA methylation
  • folate deficiency leads to genomic hypomethylation
  • hypomethylation is reversible
  • folic acid fortification in the diet results in significant decrease in incidence of open neural tube defects
115
Q

describe epigenetics and bladder cancer

A

increased methylation of the promoter site for the adhesion molecule E-cadherin

116
Q

describe epigenetics and smoking

A

down regulation of a specific DNA methyl transferase leads to demthylation of the oncogene synuclein gamma in lung tissues

117
Q

describe epigenetics and rheumatoid arthritis

A

significantly less methylation seen at IL-6 promoter site

118
Q

describe antibiotics and inflammation

A

several of the antibiotics we use for the management of periodontal disease have shown efficacy as anti-inflammatory agents

119
Q

describe doxycline and chronic ulcers in diabetic patients

A
  • characterized by elevated pro-inflammatory cytokines and proteases
  • incubation of LPS-stimulated macrophages with doxycycline totally prevented release of TNF-alpha by inhibition of TACE (TNF-alpha converting enzyme)
  • doxycycline nearly completely reduced MMP-1 (collagenase) activity
  • consistent with clinical findings
120
Q

describe minocycline and skin inflammation

A
  • doxycline evaluated for anti-inflammatory properties in acne and rosacea dermititis
  • found to have anti-inflammatory effects by inhibition of:
    • phagocytosis
    • suppression of PMN migration and chemotaxis
    • inhibition of T-lymphocyte activation
    • inhibition of phospholipase A2
    • inhibition of expression of NO synthase
    • inhibition of MMP activity
    • inhibition/stimulation of secretion of pro-inflammatory cytokines
121
Q

describe doxycline and staph exotoxin-induced cytokines and chemokines

A
  • pro-inflammatory cytokines mediate the toxic effect of superantigenic staph exotoxins (TNFalpha, IL-1, INFgamma), resulting in fever and toxic shock
  • this synergistic activity promotes tissue injury
  • tetracyclines were shown to inhibit:
    • MMP-8 and MMP-9
    • decreased elastin degradation
    • inhibited LPS induced IL-1beta production similar to that seen by corticosteroids
122
Q

describe macrolids and inflammation

A
  • for more than 20 years, it’s been known that microlids have immuno-modulatory effects in the management of several chronic inflammatory pulmonary conditions
    • suppress over abundance of PMNs by reducing chemotaxis to lungs
    • effect caused by decreasing IL-8
123
Q

describe metronidazole and colonic tissue

A

reactive oxygen species (ROS) contribute to tissue injury in inflammatory bowel diseases (IBD)

124
Q

describe the modulation of host response via nitric oxide

A
  • high levels of inflammatory conditions
  • mercaptoethyl quanidine is a NO inhibitor
  • rat model administration resulted in decreased bone loss
125
Q

describe the modulation of host response via IL-1 and TNF agonists

A
  • primate model
  • partially inhibited disease progression
126
Q

describe host modulation via the replacement/addition of pro-inflammatory interleukins

A
  • IL-4 is deficient in diseased periodontal tissues and finding that IL-4 administration in experimental arthritis reduces inflammation may be of use
  • Rh IL-11 reduced progression of periodontitis in canine model
127
Q

describe host modulation via chemically modified tetracyclines

A
  • subantimicrobial dose doxycyclines (SDD) in conjunction with ScRP
  • local delivery of minocycline may have a role
128
Q

describe host modulation via inhibition of arachidonic acid metabolite production

A
  • NSAIDS
  • triclosan (non-ionic antimicrobial)
129
Q

describe host modulation via regulation of bone metabolism

A
  • hormone replacement therapy
  • bisphosphonates
130
Q

T or F:

regulation of gene expression does not play a role in host modulation

A

false

131
Q

myth: maintenance of oral hygiene is only important to oral health.

what is the reality?

A

periodontal health is integral to systemic health, and direct links have been made between oral care and cardiovascular health, metabolic health, respiratory health, and pregnancy outcomes

132
Q

myth: periodontal care will prevent or resolve systemic health problems.

what is the reality?

A

maintaining oral health may help avoid inflammatory contributions to some systemic diseases, and treating periodontal disease may facilitate systemic health. however, periodontal treatment will not eliminate CVD, diabetes, or other systemic diseases

133
Q

myth: pregnant women should not have any dental treatment.

what is the reality?

A

maintaining oral hygiene will not endanger the health of the fetus, nor will it cause premature labor. routine dental care is not harmful to the mother or fetus during the second trimester

Perio I Supplemental Cards (7 decks)

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