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247 Periodontics > Chapters 12 & 13 > Flashcards

Chapters 12 & 13 Flashcards

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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
What happens within minutes after biofilm removal?
Free-floating microbes attach to a surface
26
What happens within 2-4 hours of biofilm removal?
Microbes form strongly attached microcolonies
27
What happens 6-12 hours after biofilm removal?
Production of ECM increases resistance
28
What happens 2-4 days after biofilm removal?
Mature colonies resistant to antibiotics; can recover from mechanical disruption within 24 hours
29
How do biofilms protect bacteria?
* 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
What action helps to maintain health by keeping bacteria in balance so no one strain can dominate?
Regular biofilm disruption
31
What are commensal bacteria?
* 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
What is the state of biofilm in health?
All epithelial-lined surfaces are colonized by biofilm
33
How are biofilms part of a mutually beneficial relationship?
* Commensal microbes contribute to host nutrition, a robust immune system and protect underlying mucous membranes * Host provides stable environment and nutrients
34
What does symbiosis mean?
Living in harmony
35
What causes oral dysbiosis?
Lack of regular disruption of oral biofilm
36
What leads to early dysbiosis?
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
What can established dysbiosis lead to?
* 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
How potent would antibitic dosages be to kill the free-floating bacteria in biofilm? Why do we not do this?
1500x stronger than systemic anibiotics Would kill the host
39
Why is mechanical distruption of biofilm essential?
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
What are two transmissible biofilm bacteria?
Aggregatibacter actinomycetemcommitans Porphyromonas gingivalis
41
Gram positive bacteria capable of colonizing the oral cavity
* Streptococcus * Actinomyces * Lactobacillus * Propionibacterium * Rothia * Peptostreptococcus * Peptococcus * Eubacterium * Bifidobacterium
42
Gram negative bacteria capable of colonizing the oral cavity
* Neisseria * Branhamella * Aggregatibacter actinomycetemcomitans * Capnocytophaga * Campylobacter * Eikenella * Haemophilus * Veilonella * Porphyromonas gingivalis * Prevotella intermedia * Tanerella forsythia * Fusobacterium * Selenomonas
43
What are the 5 phases in the formation of a biofilm?
1. Pellicle layer 2. Irriversible attachment 3. Maturation 4. Maturation II 5. Dispertion
44
What is the pellicle made of? What is it's function?
Salivary glycoproteins and antibodies Protects enamel from acidic activity
45
How is permanent attachment attained?
* By microbes that can withstand hydrodynamic forces * Microbes begin producing substances that attract other bacteria
46
What is coaggregation?
* When genetically distinct bacteria become attached to one another * Early colonizers determine which subsequent microbes colonize-- influence development of the biofilm
47
What happens in maturation phase I?
* 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
What happens in maturation phase II?
* 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
What happens in the microcolonies during maturation phase II?
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
What is quorum sensing?
* 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
What is the sequence of colonization?
* 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
What is the non-specific plaque hypothesis?
Abundant plaque adjacent to the GM led to inflammation and eventual tissue destruction
53
What are the shortcomings of the nonspecific plaque hypothesis?
* 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
What is the specific plaque/Microbial shift hypothesis?
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
What is Socransky's Microbial Complexes Hypotheis?
* 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
What are the bacterial complexes of Socransky's Microbial Complexes?
* Orange + red= major etiologic agents of periodontal disease * Yellow, green, blue and purple= associated with health
57
What are the shortcomings of the specific plaque/microbial shift hypothesis?
* 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
What are the two contemporary perspectives on the role of bacteria?
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
What is the ecological plaque hyposthesis?
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
What is the support of the ecological plaque hypothesis?
* Environment drives dysbiosis in oral cavity * Instrumentation alters the subgingival ecosystem which leads to a decrease in pathogens
61
What is the microbial homeostasis- Host response hypothesis?
* 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
What is the support of the microbial homeostasis hypothesis?
* 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
What is the Keystone Pathogen Host Response hypothesis?
* 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
What is the support for the Keystone Pathogen hypothesis?
Specific pathogens do not directly cause tissue destruction; the uncontrolled host inflammatory and immune response do

247 Periodontics (19 decks)

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