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247 Periodontics > Chapters 12 & 13 > Flashcards

Chapters 12 & 13 Flashcards

1
Q

How is oral health defined by the FDI World Dental Federation

A

The ability to speak, smile, taste, touch, chew, swallow and convey a range of emotions without pain, discomfort or disease of the cranoifacial complex

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2
Q

What does multifactorial etiology mean in terms of risk factors for periodontal disease?

A
  • Even though periodontal disease is a bacterial infection, the presence of such bacteria does not mean an individual will experience periodontitis
  • Even untreated, will not always lead to perio
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3
Q

What are the two categories of risk factors for periodontal disease?

A

Modifiable
Unmodifiable

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4
Q

What are some physical/systemic risk factors for periodontal disease?

A

Immune deficiency
Genetic Syndromes
Diabetes
Medications

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5
Q

What are some bacterial risk factors for periodontal disease?

A

A. actinomycetemcomitans
Tannerella forsythia
Porphyromonas gingivalis

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6
Q

Social and atmospheric risk factors for periodontal disease

A
  • Family, up-bringing
  • Culture
  • Socioeconomic factors
  • Access to dental care
  • Dental insurance
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7
Q

Personal habits as risk factors for periodontal disease

A
  • Self-care (plaque control)
  • Professional care (recall)
  • Smoking
  • Alcohol
  • Diet
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8
Q

What are some acquired, local, modifiable risk factors?

A
  • Plaque and calculus
  • Partial dentures
  • Open contacts
  • Overhanging and poorly contoured restorations
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9
Q

What are some anatomical, local, modifiable risk factors?

A
  • Malpositioned teeth
  • Furcations
  • Root grooves and concavities
  • Enamel pearls
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10
Q

What are some acquired, systemic, modifiable risk factors?

A
  • Smoking
  • Diabetes
  • Poor diet
  • Certain medications
  • Stress
    Emerging: nutrition, alcohol, obesity
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11
Q

What are some non-modifiable risk factors?

A
  • Socioeconomic status
  • Genetics
  • Adolescence
  • Pregnancy
  • Age
  • Leukemia
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12
Q

What is the most significant known risk factor for periodontitis?

A

Cigarette smoking

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13
Q

Why do many patients who present at every hygiene visit w/ generalized biofilm have gingivitis that never progresses to periodontitis?

A

Their immune system effectively deals w/ the periodontal pathogens and any related risk factors

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14
Q

Why does gingivitis progess to periodontits in some individuals?

A

Their immune response is responsible for the tissue destruction seen in periodontitis and they may have systemic risk factors that increase their susceptibility

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15
Q

What is some demographic data that is included in the clinical risk assessment?

A
  • Age
  • Duration of exposure to risk factors
  • Self-care
  • Frequency of dental visits
  • Male gender
  • Dental awareness
  • Socioeconomic status
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16
Q

What is some medical history information used in the clinical risk assessment?

A
  • Tobacco use
  • Diabetes
  • Osteoporosis
  • HIV/AIDS
  • Genetic predisposition to aggressive disease
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17
Q

What is some dental history information used in the clinical risk assessment?

A
  • Frequency of professional care
  • Family history of early tooth loss
  • Previous history of periodontal disease
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18
Q

Clinical examination factors included in the clinical risk assessment

A
  • Plaque biofilm accumulation and microbial composition
  • Calculus deposits
  • BOP
  • Loss of attachment
  • Plaque retentive areas
  • Anatomic contributing factors
  • Restorative contributing factors
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19
Q

Characteristics of gram positive bacteria (purple stain)

A

Single, thick multilayered cell wall of peptidoglycan lying above the cytoplasmic membrane

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20
Q

What is peptidoglycan?

A

Sugars and amino acids

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21
Q

Characteristics of gram negative bacteria (red stain)

A

Two membranes sandwiching a thin cell wall of peptidoglycan
Outer= proteins and lipopolysaccharide (endotoxin/play major role in pathogenesis of gram neg infections)
Inner= cytoplasmic membrane

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22
Q

What are microbial communities?

A
  • Microorganisms tend to live in complex communities attached to surfaces
  • Not free-floating
  • Contain different species and are spacially organized
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23
Q

What are biofilms?

A

Complex, dynamic microbial community w/ bacteria, fungi and viruses embedded in a self-protective matrix adhered to a surface
Microbes synthesize the protective matrix
Can exist on any solid surface that is exposed to microbe-containing fluid

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24
Q

What percentage of all diseases may be biofilm induced?

A

65%

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25
Q

What happens within minutes after biofilm removal?

A

Free-floating microbes attach to a surface

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26
Q

What happens within 2-4 hours of biofilm removal?

A

Microbes form strongly attached microcolonies

27
Q

What happens 6-12 hours after biofilm removal?

A

Production of ECM increases resistance

28
Q

What happens 2-4 days after biofilm removal?

A

Mature colonies resistant to antibiotics; can recover from mechanical disruption within 24 hours

29
Q

How do biofilms protect bacteria?

A
  • Blocking:ECM may block small molecules
  • Mutual protection: cooperation btw bacteria. Normal flora may block pathogens from adhering/joining biofilm
  • Hibernation: Protective quiescence against antibiotics
30
Q

What action helps to maintain health by keeping bacteria in balance so no one strain can dominate?

A

Regular biofilm disruption

31
Q

What are commensal bacteria?

A
  • Bacteria that act upon the hosts immune system to induce protective responses that prevent coloinzation and invasion by pathogens
  • Part of the normal flora
32
Q

What is the state of biofilm in health?

A

All epithelial-lined surfaces are colonized by biofilm

33
Q

How are biofilms part of a mutually beneficial relationship?

A
  • Commensal microbes contribute to host nutrition, a robust immune system and protect underlying mucous membranes
  • Host provides stable environment and nutrients
34
Q

What does symbiosis mean?

A

Living in harmony

35
Q

What causes oral dysbiosis?

A

Lack of regular disruption of oral biofilm

36
Q

What leads to early dysbiosis?

A

Imbalance of microbial colonies due to lack of regular disruption–> Starts to favor bacterial species which elicit a stronger host response, which in turn leads to the development of gingival inflammation

37
Q

What can established dysbiosis lead to?

A
  • In oral cavity–> periodontits
  • Gradual change of symbiotic host-microbe relationship to a pathogenic one
  • Triggers host response in a susceptible patient
  • Leads to tissue damage
38
Q

How potent would antibitic dosages be to kill the free-floating bacteria in biofilm?
Why do we not do this?

A

1500x stronger than systemic anibiotics
Would kill the host

39
Q

Why is mechanical distruption of biofilm essential?

A

Forces bacteria to start over with initial attachment and move through the stages to become a mature biofilm

Areas cleaned regularly will not develop mature biofilms

40
Q

What are two transmissible biofilm bacteria?

A

Aggregatibacter actinomycetemcommitans
Porphyromonas gingivalis

41
Q

Gram positive bacteria capable of colonizing the oral cavity

A
  • Streptococcus
  • Actinomyces
  • Lactobacillus
  • Propionibacterium
  • Rothia
  • Peptostreptococcus
  • Peptococcus
  • Eubacterium
  • Bifidobacterium
42
Q

Gram negative bacteria capable of colonizing the oral cavity

A
  • Neisseria
  • Branhamella
  • Aggregatibacter actinomycetemcomitans
  • Capnocytophaga
  • Campylobacter
  • Eikenella
  • Haemophilus
  • Veilonella
  • Porphyromonas gingivalis
  • Prevotella intermedia
  • Tanerella forsythia
  • Fusobacterium
  • Selenomonas
43
Q

What are the 5 phases in the formation of a biofilm?

A
  1. Pellicle layer
  2. Irriversible attachment
  3. Maturation
  4. Maturation II
  5. Dispertion
44
Q

What is the pellicle made of? What is it’s function?

A

Salivary glycoproteins and antibodies

Protects enamel from acidic activity

45
Q

How is permanent attachment attained?

A
  • By microbes that can withstand hydrodynamic forces
  • Microbes begin producing substances that attract other bacteria
46
Q

What is coaggregation?

A
  • When genetically distinct bacteria become attached to one another
  • Early colonizers determine which subsequent microbes colonize– influence development of the biofilm
47
Q

What happens in maturation phase I?

A
  • When firmly attached bacteria secrete protective ECM or extracellular polymeric substance
  • Matrix protects the microbes from host immune defenses and antibiotics–> establishment of chronic disease state
48
Q

What happens in maturation phase II?

A
  • Microcolony formation: microbial blooms (specific bacteria grow at accelerated rates)
  • Mushroom shaped microcolonies attach to the tooth by a narrow base
  • Diverse populations ensure survivability and are less likely to be destroyed by toxic agents
49
Q

What happens in the microcolonies during maturation phase II?

A

Internal organozation of mature biofilm:
* Layers of microbes
* Fluid channels (direct nutrients and O2 and remove waste)
* Cell-to-cell communication- chemical signals btw microcolonies- gene transfer btw microbes

50
Q

What is quorum sensing?

A
  • Bacterial signaling– microbes release and sense small proteins used to trigger cellular adhesion, formation of matrix
  • Bacteria share info helping them to adapt and coordinate behavior
51
Q

What is the sequence of colonization?

A
  • Early colonizers adhere to pellicle- streptococcus, S. mitis, S. oralis
  • Release chemical signals (quorum sensing)
  • Free-floating microbes join once conditions are favorable in “alphabetical order”
52
Q

What is the non-specific plaque hypothesis?

A

Abundant plaque adjacent to the GM led to inflammation and eventual tissue destruction

53
Q

What are the shortcomings of the nonspecific plaque hypothesis?

A
  • Too simplistic
  • More questions need to be asked: why do some plaque laden patients never develop perio? Why do some pts w/o plaque develop perio? Why are not all sites affected equally, and some not at all?
54
Q

What is the specific plaque/Microbial shift hypothesis?

A

The composition of the plaque rather than the amount is the deciding factor. A shift from non-pathogens to pathogens, from g(+) to g(-) anaerobes

55
Q

What is Socransky’s Microbial Complexes Hypotheis?

A
  • Specific groups of bacteria significantly associated w/ periodontitis: T dentiola, T forsythia, P gingivalis
  • Groups either pathogens or non-pathogens
  • Bacteria assigned to complexes by color
56
Q

What are the bacterial complexes of Socransky’s Microbial Complexes?

A
  • Orange + red= major etiologic agents of periodontal disease
  • Yellow, green, blue and purple= associated with health
57
Q

What are the shortcomings of the specific plaque/microbial shift hypothesis?

A
  • Red complex bacteria T forsythia and P gingivalis can be found in healthy sites
  • There are over 700 other organisms that have been shown to correlate better with perio disease than typical “red complex”, 200-700 of which may be present in the pts oral cavity
58
Q

What are the two contemporary perspectives on the role of bacteria?

A
  1. Pathogenic microbial biofilm is a prerequisite for perio to develop but presence of it alone is insufficient to cause the disease
  2. Red complex microorganisms are strongly associated w/ inflammatory disease but there is no current evidence that they are potent initiators of the disease
59
Q

What is the ecological plaque hyposthesis?

A

Accumulation of nonspecific bacteria lead to an inflammatory response
Inflammatory response leads to alteration of local environment (^ GCF, bleeding, pH and decrease of O2)
Environment more conducive to specific pathogenic bacteria

60
Q

What is the support of the ecological plaque hypothesis?

A
  • Environment drives dysbiosis in oral cavity
  • Instrumentation alters the subgingival ecosystem which leads to a decrease in pathogens
61
Q

What is the microbial homeostasis- Host response hypothesis?

A
  • Biofilms cause initial inflammatory response but pathogenic bacteria are not the direct cause of tissue destruction
  • Focus is on host immune response
  • Genetic variation and immune response are recognized as major factors in initiation and progression
62
Q

What is the support of the microbial homeostasis hypothesis?

A
  • Microbe population associated w/ health remains stable over time
  • Some potential pathogens identified have not been shown to be directly responsible for perio tissue destruction
  • Overwhelming evidence demonstrates uncontrolled host inflammatory/immune response (not pathogens) cause tissue destruction
63
Q

What is the Keystone Pathogen Host Response hypothesis?

A
  • P. Gingivalis–> “keystone species” initiating shift from symbiotic to dysbiotic microbes
  • Present in small numbers, keystone exerts large effect
  • Transition requires both polymicrobial dysbiotic biofilm + susceptible host
64
Q

What is the support for the Keystone Pathogen hypothesis?

A

Specific pathogens do not directly cause tissue destruction; the uncontrolled host inflammatory and immune response do

247 Periodontics (19 decks)

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