Chronic Periodontitis and Atherosclerotic Vascular Disease Flashcards
Does what happens in the oral cavity stay in the oral cavity?
• Implications periodontitis may have on someone developing atherosclerotic disease • Common clinical scenarios ○ Advanced perio ○ Edno ○ Severe caries ○ PA abscess ○ Perimplantitis ○ Gingival inflammation, recession > perio • All these have inflammation, all have \_\_\_\_ etiology • Inflam response > breakdown of apparatus ○ Bacterial infection in mouth and inflam response in mouth > manifests systemically
microbial
• L: no decay, and no loss of attachment
○ May be resistant
• LM: severe dental decay; no recession around the roots; no periodontitis, no attachment loss
○ This patient seems to susceptible to caries, but resistant to periodontal disease
• RM: clinically, decent oral hygiene, but in the x-rays > severe attachment loss (severe inflammation)
○ This patient was originally 17 y/o
• R: chronic periodontitis
○ Some caries
○ Her gingiva: edematous, erythema, unhealthy gingiva
○ Radiographs - severe bone loss
• Why the difference between the four?
○ Different bacteria in each different mouth, but the bugs that cause them are thought to be outgrowths of our normal flora
○ Differences in patients diet
○ Different type of ____
○ Different ____
• BL: dental implant placed > significant amount of bone loss around the implant > perimplantitis
○ Can get bone loss around implants, similar to how it happens in natural teeth
○ Soft tissues are highly inflamed > it is responsible for inducing the bone loss
immune responses
genetics
Evolution of the Focal Infection Theory
- Hippocrates “cures” ____ by extracting a tooth.
- W. D. Miller (1890) proposed that certain “general” infections were caused by oral infections and advised endodontic therapy on carious teeth. First used the term “____” in 1891.
- Frank Billings (1911) published case reports claiming to have cured infections of “distant organs” via ____ and tooth extractions.
- A 1926 report in Dental Cosmos advocated extraction of known healthy teeth to prevent ____.
arthritis
focal infection
tonsillectomies
focal infection
Evolution of the Focal Infection Theory
- From 1930 through the 1950s the theory came under attack by both the medical and dental communities resulting in it being abandoned.
- James Dunning (1986): “in spite of a decline in recognition of the focal infection theory, the association of ____ with systemic disease is taken very seriously”.
- A number of papers are published in the early 1990s proposing an association between dental disease and ____.
dental decay
heart disease
“Revised” Focal Infection Theory
“The focal infection theory posits that bacteria and/or bacterial toxins and metabolic by- products can enter the systemic circulation from a clinically asymptomatic localized lesion that contains pathogenic bacteria and translocate to distant parts, initiating disease in these other organ systems. The resulting metastatic disease is chronic, but not ____.”
“…..the underlying pathophysiology of systemic diseases caused by periodontal infections may be metastatic infection, metastatic injury or metastatic inflammation.”
• Components of focal infection is actually true • Not infectious is the chronic sense of infectious disease • Only problem - "systemic diseases casued by perio infections" ○ Perio disease doesn't cause \_\_\_\_ § This has not been proven!
systemic disease
Chronic Periodontitis and Systemic Disease
• What can happen in mouth and how affects systemic health • Periodontitis and CV disease • Periodontal and respiratory, \_\_\_\_ (well known), OP, RA, and more recent: ED, \_\_\_\_-complications, oral cancer, neurologic (stroke, ALZ, dementia, depression) ○ Studying associations is what field of periodontal medicine is about • In 90's > dramatic increase regarding association ○ Show perio is a risk for \_\_\_\_ > how can we intervene? § \_\_\_\_ and eliminate risk factors is the major way of preventing disease
diabetes
pregancny
CAD
proactive
How is a relationship between two diseases evaluated?
• How do evaluate the associaiton? ○ Through clinical research, and biologic mechanisms (via looking at animalmodels and bench work) • Clinical studies that can be done ○ Types of evidence that can exist in literature bet two entities § \_\_\_\_: papers describe patients § \_\_\_\_: § \_\_\_\_: patients over protracted § \_\_\_\_: treat patients □ Biggest problem: looking at perio with ASVD > would have to identify a population with perio disease, and need a control; and then, the patients with perio, need one that you treat and one that you don't treat; and then, ask the question do they develop disease □ To do studies like this: need \_\_\_\_, and need a lot of money □ Do not have a lot of these, because you may not wait enough for it to develop § Systematic review ○ The strongest level: \_\_\_\_; the least strenght is the \_\_\_\_ § SR says that something is true, then its true § There's a right and wrong way to do a SR; any clinical dental journal will have a SR in it § Have to rely on the \_\_\_\_ ones, because SR are not always done properly § \_\_\_\_ have the potential to being most informative
case reports cross-sectional longitudinal intervention trials clinical facility SR case reports middle intervention trials
How is a relationship between two diseases evaluated?
Risk Factor (Risk Determinant): A variable associated with an increased risk for a disease or infection.
- correlational associations that are not necessarily causal - appropriate studies/statistical analysis are necessary to
assess the strength of the association and prove causality
• If able to carry out a study: ○ Four situation that develop: § Prove that disease casues this disease: he \_\_\_\_ □ Chronic perio is not known to cause any systemic disease § Positive association with one another: he \_\_\_\_ □ If 5-10X more likely > very significant, not as much as 1.5 § he \_\_\_\_ against disease □ Chronic perio doesn't do that § he \_\_\_\_ □ There is a situation in chronic perio and diabetes ® Uncontorlled diabetes > periodontla disease ® Perio disease > glycosylated hemoglobin levels • Studies identify risk factors
causal
associatied
protection
bidirecional
Risk Factors for Chronic Periodontitis and Atherosclerotic Vascular Disease
Periodontitis:
- ____
- ____
- ____
- ____
- ____
- Medications
- Clenching/Grinding Teeth
- Poor ____
ASVDs:
- ____
- ____
- ____
- ____
- Hypercholesterolemia - Dyslipidemia
- ____
- Poor ____
- Inactive Lifestyle
- Alcohol• Share major risk factors
• One explanation in relationship: can get both diseases, showing an association between the two
○ The ____ is stronger than simply sharing risk factors
age genetics smoking/tobacco use diabetes stress nutrition/obesity
age genetics (race/sex) smoking/tobacco diabetes stress poor nutrition/obesity
association
Is a relationship between chronic periodontitis and atherosclerotic vascular disease biologically plausible?
• ASVD in lay terms: plumbing problem > the coronaries clogged, clots into cerebral vasculature and you got strokes • Formation of \_\_\_\_ ○ Accumulation of macrophages, clotting factors, migration of cells into the connective tissue > inflammation • \_\_\_\_ in mouth in periodontitis, and may get into systemic circulation and can affect any body compartment in your body ○ Does it explain association between the diseases?
atheroma
inflammation
Current Paradigm of Periodontal Pathogenesis
HOMEOSTASIS
Even within clinical healthy gingiva there is ample histologic evidence of a ____ to various components of the symbiotic microflora.
This physiological inflammatory state or ‘armed peace’ is the result of host interactions with ____ bacteria which are in close contact with (but do not invade) the periodontal tissues.
• If saw a patient with good healthy gingiva > made assumption, at microscopic view > no indications of inflammatory reaction ○ Not the case > reads the first bullet ○ Always a low level of \_\_\_\_ occurring, even in healthy gingiva ○ Efflux of \_\_\_\_ from undelrying CT to the gingival sulcus, stimluated by plaque bacteria found even on healthy teeth § Reads next point § Prevents bacteria moving from \_\_\_\_ of body to the inside • Periodontal health represents a state of homeostasis that is maintained by this low level \_\_\_\_ reaction
host response commensal bacteria inflam neutrophils outside inflam
Current Paradigm of Periodontal Pathogenesis
• Slide in context of ecologic plaque hypothesis ○ If plaque reduciton kept in tact, minimal inflammation, microbiota that develops in plaque is \_\_\_\_ and is associated with periodontal health • Stop brushing and flossing > inflammation > plaque acuum > increase in inflam > enviornemtnal changes in perio enviro > \_\_\_\_induced > outcome is \_\_\_\_ supragingival plaque > induciton of gingivitis ○ All driven by change in microflora that induces inflammation, and likes inflamed sites to live in • Doesn't get teeth cleaned, poor oral hygiene > under conditions of inflam > creates situationt aht faciliates growth of unique bacteria > \_\_\_\_ (keystone pathogen) - the bug is not found at high levels and doesn't breakdown the apparatus, but changes environemental and developing an ecological situation that allows growth of additional pathologic species of bacteria ○ At this occurs > increase inflammation, and many of bacteria involved in pathogenesis of periodnotis > live in \_\_\_\_ enviornement, and they're \_\_\_\_, and can tolerate/like highly inflamed areas > as increase in level of inflammation > second ecological shift > disease provoking \_\_\_\_ microbiota > involved in pathogenesis of periodontittis > more inflammation > another transistion > accum of \_\_\_\_ pathogens, further enhancing inflammation > breakdown of apparatus can continue unless you break change events
symbiotic
inflammation
mature
p gingivalis subgingival proteolytic inflammophilic accessory
Current Paradigm of Periodontal Pathogenesis
Pro-Inflam mediators IL1B TNFalpha IFNgamma RANKL IL17 PGE2 MMPs
Anti-inflam mediators IL1ra IL10 osteoprotegrin TGFb TIMPS
* As a result to this, dramatic changes in the types of cytokines that are found in GCF > perio healthy > high levels of anti inflam mediators; and otherwise, in perio: pro-infla mediators (IL7, RANKL induces osteoclastogenesis (bone resorption) * GCF comes from \_\_\_\_ - they're in the local circulation in the mouth > can get into serum in other parts of body
serum
Current Paradigm of Periodontal Pathogenesis
Today, it is increasingly recognized that periodontal diseases are not bacterial infections in the classical sense, i.e., caused by a ____ or a limited number of exogenous pathogens.
Relevant organisms are likely a component of the ____ oral flora albeit in very low numbers at healthy sites and ____ in abundance at diseased sites. The bacteria are necessary for but not ____ to cause disease.
Gingivitis results from a build-up in the plaque mass that is, in part, due to the accumulation of \_\_\_\_ bacteria leading to the induction of an inflammatory reaction that may be of a sufficient magnitude to “control” the biofilm. Periodontitis is the result of a \_\_\_\_ community-induced perturbation of host homeostasis leading to inflammation in susceptible individuals. • In order to have disease > induction of inflam reaction and host repsonse > host response is repsonsible for degradation of attachment apparatus
single
normal
increasing
sufficient
gram-negative
polymicrobial
Current Paradigm of Periodontal Pathogenesis
Interactions between bacteria and both the ____ components of the host’s immune system are central to the pathogenesis of periodontal disease.
Tissue damage can result via the direct effects of bacterially-derived substances that impact the viability of host cells and integrity of host tissues or indirectly, by induction of an ____ reaction on the part of the host.
Certain bacterial constituents of the polymicrobial plaque community often exhibit \_\_\_\_ interactions that will enhance colonization, persistence or virulence. Some bacteria may be involved in the breakdown of \_\_\_\_ whereas others may trigger \_\_\_\_ inflammation once homeostasis is disrupted. Susceptibility to and progression of disease is modulated by both \_\_\_\_ factors
innate and adaptive inflammatory/immunlogic synergistic homeostasis destructive inflammation intrinsic and extrinsic
