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Perio Risk Assessment Flashcards

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1
Q

Definition of Gingivitis

A

INFLAMMATION of the gingiva as a response to bacterial plaque on adjacent teeth; characterized by erythema, edema, and fibrous enlargement of the gingiva WITHOUT RESORPTION OF UNDERLYING ALVEOLAR BONE

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2
Q

definition of periodontitis

A

inflammation of the periodontium
chronic inflammation occuring in the response to plaque on the adjacent teeth; characterized by gingivitis destruction of the alveolar bone and pdl, APPICAL MIGRATION OF EPITHELIAL ATTACHMENT resulting in the formation of periodontal pockets, ultimately loosening and exfoliation of the teeth

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3
Q

what is essential for the initiation of periodontal inflammation and disease

A

PLAQUE

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4
Q

experimental gingivits in man - general idea and what it provided us?

A

experiment that showed that plaque / bacteria is the main etiologic role in periodontal disease

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5
Q

experimental gingivits in man three steps

A
  1. preparatory phase – intense plawue control
  2. period of no plaque control – plaque accumulares and onset of build up ensues
  3. plaque control is resumed - volunteers are able to resume plaque control and the influence of plaque removal on the experimental gingivitis is followed
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6
Q

findings from experimental gingivits in man

A

time necessaary to develop gingivitis varied from ten to twenty one days

all subjects developed accumulations of soft debris and the development of marginal gingivitis

number of microorganisms in gingival area increased and distinct changes in relative composition of the gingival flora occured

reinstitution of oral hygein resulted in a return to healthy gingival conditions and reastablishment of the original bacterial flora

*gingivitis CAN BE EXPERIMENTALLY PRODUCED and gingivitis CAN BE COMPLETELY REVERSED

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7
Q

primary etiologic factor for inflammatory perio disease?

A

DENTAL PLAQUE – however might not be enough alone

RISK factors appear to be critical in helping to determine who develops the diseas, the severity of the disease, the response to therapy and the rate of reaccurence

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8
Q

what’s determined in assessing risk?

definition of risk assessment?

A

probability that a disease outcome will occur following a particular exposure is estimated

risk assessment is a way of examining risks so that they may be avoided, reduced, or managed

risks can be identified in terms of risk factors, risk indicators, or risk predictors

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9
Q

two criteria for being a risk factor

A
  1. it is biologically plausible as a causal agent for disease
  2. it has been shown to preceed the development of disease in PROSPECTIVE (forward design) clinical studies
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10
Q

risk indicator?

A

a factor that IS BIOLOGICALLY plausaible as a causitivie agent for diease but has only been associated with disease in CROSS-SECTIONAL STUDIES

may be proven to be risk factor IF PROSPECTIVE STUDIES are able to confirm they precede the development of disease

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11
Q

is herpesviruses n subgingival plaque a perodontal disease risk indicator or factor?

A

INDICATOR – although biologically plausible as a causitive agent in perio disease – only research in cross-sectional studies

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12
Q

what is a risk marker?

A

usually ASSOCIATED with a risk factor but NOT a factor themselves or in the causative pathway

  • no current biological evidence as a causitive agent - but associated with disease on cross-sectional or longitudinal basis
  • may be either markers for disease or other historical measures of disease
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13
Q

risk marker example?

A

example of a risk marker – could be a PREDICTOR of disease but has LITTLE OR NO biological plasibility as a causitivie agent for periodontitis

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14
Q

two types of risk factors for periodontal disease - general w/ examples

A
  1. local factors - like overhanging restorations and root caries that allow for plaque accumulation, pocket depth, intra-bony pockets involving furcations and endo infections
  2. systemic factors - smoking, diabetes, genetic factors
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15
Q

are risk factors modifiable?

A

YES - some are but some genetic ones are not

smoking - yes
overhang restorations - yes you can remove these

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16
Q

explain levels of exposure to risk factors and give examples

A

often - clear dose dependent response

linear relationship in both smoking and diabetes

smoking with levels of bone loss and diabetes with severity of perio disease

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17
Q

explain the concept of threshold

A

for many risk factors - it is believed that there is a threshold below which the factor in question has a negligible clinical effect on the disease process – but ONCE THRESHOLD IS CROSSED THERE IS A CONSIDERABLE INCREASED RISK FOR THE DISEASE

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18
Q

what acts as plaque retentive factors?

A

local risk factors as they increase the risk of development and progression of periodontal disease by acting as these plaque retentive factors

*removal of local risk factors should be included in the patient’s treatment plan

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19
Q

list examples of local risk factors

A
  1. anatomical factors – like enamel pearls, projections, cemental tears, root grooves, tooth poisiton , malocclusion, open contacts
  2. restorations - rough, subgingival, marginal discrepencies, under/over contoured
  3. removable partials
  4. ortho appliances
  5. root fractures and cervical root resorption
  6. calculus
  7. local trauma
  8. frenal attachments
  9. mouth breathing/ lack of lip seal
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20
Q

trauamtic occlusion association with perio?

A

poorer perio prognosis following therapy

  • presence of decrease in the crestal bone height
  • more increased poor prognosis if not using a night guard
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21
Q

teeth that respond best and worse to perio therapy?

A

frequently lost –> maxillary second molars

highest retention –>mandibular canines and and first pre-molars

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22
Q

what forms on top of plaque

A

calculus always forms on top of plaque

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23
Q

what is supragingival calculus often associated with?

A

gingivitis and gingival recession

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24
Q

subgingival calculus
describe it
associated with?

A

it has an irregular porous surface and can act as a reservoir for periodontal pathogens and endotoxins

this and its associated plaque layer is associated with the development of periodontitits and hgher rates of disease progression

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25
distribution of supragingival calculus
around the openings of salivary glands lingual on mandibular anteriors buccal by maxillary second molar
26
distribution of SUBragingival calculus
not really predictable but more associated with lingual and interproximal sites over buccal sites
27
appearance of supragingival calculus
creamy-white to yellow, may pick up extrinisic stains
28
appearance of subgingival calculus
brownish-black
29
mineral content and source in supragingival calculus
mean of 37% by volume, derived FROM SALIVA
30
mineral content and source in SUBragingival calculus
mean of 58% by volume and derived from the GCF
31
crystal type in supragingival mineral content and source in supragingival calculus
mostly octacalcium phospate and hydroxyapatite some whitlockite very little brushite
32
crystal type in SUBragingival mineral content and source in supragingival calculus
whitlockite is the major constituent; it develops under anaerobi, alkiline conditions in the presence of Mn, Zn, and carbonate hydroxyapetite is also present and some octacalcium phosphate NO brushite
33
oral hygeine has a clear causal relationship with what?
gingivitis - relationship b/w oral hygeine and periodontitis is less straightforward
34
oral hygiene role in microbial flora
can favorably influence the ecology of microbial flora in shallow-to moderate pockets - but does not effect the host response has little effect on subgingival microflora in deep pockets and personal oral hygeine practices among health professionals have been shown to be unrelated to periodontitis in those individuals
35
bacteria in supragingival plaque can do what if bacteria insult is strong enough??
when enough to overwhelm the host defense - they can migrate subgingivally to form a subgingival biofilm but frequent professional cleaning and good oral hygeine has been shown to have a beneficial effect on subginigval mcrobiota in moderatley deep pockets
36
systemic risk indicators or putative risk factors for perio?
low dietary calcium intake, postmenopausal osteoporosis and osteopenia, stress
37
smoking does what to the inflammatory and immune response?
exaggerate the inflammatory response and suppress the immune response
38
local effects of smoking
direct toxicity to cells, thermal effects, increased stain and calculus formation, and effects on the oral flora. smoking has also been shown to negatively affect bone mineral density
39
smoking true risk factor for perio?
YES
40
odds ratio for smoking and perio disease? heavy smokers? light smokers?
2-7 is the range heavy smokers have 2x the odds of a light smoker as well in terms of bone loss and attachment loss
41
T/F smoking is a risk factor that is independent of oral hygeine, age, or other factos
TRUE | - exactly how it acts in the causal change is still up for debate
42
smoking association with plaque? | w/ perio pathogens subgingivally?
plaque accumulation shows mixed results with some increased and some with no difference may be associated with higher prevelence of these bacteria but maybe not higher proportions
43
gingival vascularity in smokers?
in smokers was seen to be only half that seen in non-smokers - smoking suppresses hemorrhagic response as measured by BOP - masking effect of inflammation
44
what does smoking promote the production of?
TNF alpha and the release of cytokines
45
what are the true risk factors for perio?
1. smoking --> even stronger than diabtes | 2. diabetes
46
when does type 1 and type 2 diabetes begin?
1--> early onset w/ complete destruction of beta cells 2--> later onset and associated with obesity and has impaired insulin function and relative deficiency
47
common complications associated with diabetes
``` retinopathy nephropathy neuropathy vascular disease altered wound healing ```
48
T/F studies have shown an association with uncontrolled diabetes / diabetes with attachment or periodontal bone loss
TRUE
49
diabetes implication on infections?
decreased immune response and thus an increased susceptibility to infection -- thus increased risk for periodontal disease
50
what have twin studies shown us?
there is a significant genetic component in chronic periodontitis in adults 38%-82% of variance seen in gingivitis, pribing deoth, and clinical attachment loss is due to genetic variaiton
51
what gene is associated with more severe periodontitis?
polymorphic IL-1 gene - but could only be demonstrated in non-smokers - thus this is not as strong of a risk factor than smoking
52
IL-1 significance?
specific genotype of this is related to increased risk of perio - makes sense because this is a PRO-INFLAMMATORY CYTOKINE which is a KEY REGULATOR OF HOST RESPONSE to microbial infection HAS BEEN IDENTIFIED AS A CONTRIBUTORY CAUSE OF PERIODONTITIS
53
what do individuals who are genotype positive for IL-I produce?
they produce 2-4 times more IL-IBeta than individuals who are genotype negative
54
when trying to confirm association of IL-1 in studies what do they find?
specific environmental factors are such strong risk factors that they overwhlem any genetically determined susceptibility or resistance to disease - hard to confirm associations but some have been found
55
which is higher priority stop smoking or genetic testing for IL-1?
STOP SMOKING
56
AGE relationship with prevelance and severity of CAL? PD?
INVARIABLY related directly in cross-sectional studies - so CAL does increase with age but not directly related to loss of function in the affected teeth PD - also related to age but less directly BUT NOT A DISEASE OF AGING - greater periodontal destruction in the elderly as reflecting lifetime disease accumulation rather than an age-specific condition
57
T/F it is uncommon for elderly people with reasonably intact dentition to exhibit sudden bursts of periodontitis
TRUE the tooth retention, good oral hygiene, and periodontal health (exhbited by little gingival inflammation and few deep pockets) are closely associated, regardless of age
58
Gender and implication on CAL?
CAL and levels of severity more prevelant in MALES than females - males usually exhibit poorer oral hygiene than females, whether measured as calculus or soft plaque deposits
59
when are females 'more' susceptible to perio complications?
- post-menopausal (loss of the protective function of estrogen) - hormonal conditions like pregnancy associated perio - puberty associated gingivitis (can affect both genders)
60
Socioeconomic status?
generally, those with better education, wealth, health status have less liklihood of periodontal disease - so perio disease related to lower SES RELATIONSHIP IS PROBABLY RELATED TO BETTER ORAL HYGIENE, BETTER EDUCATION, MORE FREQUENT DENTAL VISITS, AND INSURANCE
61
Socioeconomic status relationship to oral hygiene, gingivitis, and periodontitis?
oral hygiene and gingivitis clearly related to SES relationship to periodontitis and SES is less direct
62
racial / ethnic differences relationship to perio disease?
more likely related to these groups and SES rather than the genetic differences within these groups so a complex, multi-faceted variable that can include a variety of cultural factors
63
osteoporosis implication
related to increased dental calculus and indicator for CAL and gingival recession NOT for increased pocket depth - confirmed that osteoporosis in women is a ris factor for loss in alveolar bone density --> likely related to reduced estrogne levels which lead to resorption outpacing bone deposition , which sets the stage for more advanced periodontal bone loss associated with perio infections
64
stress and inadequate coping implication?
chronic stress and increased allostatic load appear to have many deleterious effects on host including supression of the immune response with increased susceptibility of infections LIKE PERIO DISEASE

Periodontology (20 decks)

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