Path pt1 Flashcards

1
Q

What role do bacteria play in periodontal disease?

A

Bacteria are pivotal in periodontal disease development. A few specific species among hundreds in the oral cavity are linked to disease. Dysbiosis, a shift in microbial balance, leads to disease.

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2
Q

What is the acquired enamel pellicle and why is it important?

A

A protein layer formed from saliva that coats enamel within 1 minute. It provides adhesion sites for bacteria and is the foundation for biofilm development.

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3
Q

What are the primary colonizers in dental biofilm formation?

A

Streptococci dominate early colonization. They are obligate aerobes and prepare the environment for anaerobes by depleting oxygen.

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4
Q

What are the main phases in dental biofilm formation?

A
  1. Pellicle formation, 2. Initial bacterial adhesion, 3. Colonization/biofilm maturation.
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5
Q

How does subgingival biofilm differ from supragingival biofilm?

A

Subgingival biofilm is anaerobic and rich in gram-negative rods and spirochetes; supragingival biofilm is stratified with gram-positive cocci near tooth and gram-negative on outer surface.

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6
Q

What is the nonspecific plaque hypothesis?

A

States that disease is due to overall plaque accumulation, regardless of bacterial composition. Later disproven by epidemiological studies.

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7
Q

What is the specific plaque hypothesis?

A

Suggests that specific pathogenic bacteria (like red complex bacteria) are responsible for periodontitis, rather than total biofilm volume.

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8
Q

What is the ecological plaque hypothesis?

A

Unifies prior theories; both biofilm quantity and microbial composition, influenced by host/environmental factors, can cause dysbiosis and disease.

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9
Q

What is the red complex of periodontal pathogens?

A

A group of bacteria—T. forsythia, P. gingivalis, T. denticola—strongly associated with periodontitis and deep probing depths.

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10
Q

What is dental calculus and how is it formed?

A

Calcified dental plaque. Supragingival calcifies via salivary minerals; subgingival via gingival crevicular fluid. Can form in 4–8 hours.

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11
Q

Where is supragingival calculus commonly found?

A

Buccal surfaces of maxillary molars and lingual surfaces of mandibular incisors—areas near salivary ducts.

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12
Q

How is subgingival calculus detected and characterized?

A

Detected by tactile exploration. Hard, dark-colored, and adherent. Does not reach the junctional epithelium.

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13
Q

What are the four modes of calculus attachment to teeth?

A
  1. Organic pellicle, 2. Mechanical locking into surface irregularities, 3. Close adaptation to unaltered cementum, 4. Bacterial penetration into cementum.
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14
Q

What is the clinical significance of subgingival calculus?

A

It retains plaque, aggravating inflammation. It’s not the cause of disease, but a perpetuating factor. Removal is critical to therapy.

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15
Q

What are local predisposing factors for periodontal disease?

A

Restorative margins, tooth contour issues, piercings, and defects distal to second molars post-third molar extraction.

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16
Q

What are the three major ecological niches in the oral cavity?

A

1) Shedding surfaces (oral mucosa), 2) Non-shedding surfaces (teeth, implants), and 3) Subgingival areas (like periodontal pockets).

17
Q

What characteristics of teeth and implants allow for mature biofilm formation?

A

They are hard, non-shedding surfaces that permit long-term bacterial adhesion and biofilm development.

18
Q

What is the role of saliva in biofilm development?

A

Though antimicrobial, saliva helps bacteria adhere via glycoproteins in the acquired pellicle and supplies nutrients that support bacterial growth.

19
Q

What is coadhesion and why is it important in biofilm maturation?

A

It’s the binding of secondary colonizers to primary ones, enabling microcolony development and mature biofilm structure.

20
Q

How quickly does the pellicle form on enamel after cleaning?

A

Within 1 minute, and it reaches a dynamic equilibrium by 2 hours.

21
Q

How does dysbiosis relate to periodontitis?

A

Dysbiosis is an imbalance in the microbial community, favoring pathogenic anaerobes, which contributes to chronic inflammation and periodontal destruction.

22
Q

What is the significance of the redox potential in subgingival biofilms?

A

Low redox potential favors anaerobic bacterial growth, a key factor in periodontitis pathogenesis.

23
Q

How do host leukocytes interact with the apical portion of mature subgingival biofilm?

A

A leukocyte-rich layer separates the biofilm from the junctional epithelium, helping contain bacterial invasion.

24
Q

What does the presence of dark supragingival calculus imply?

A

It suggests possible gingival recession exposing previously subgingival calculus, which may now be visible.

25
How is materia alba different from plaque?
Materia alba is an unorganized mass of bacteria, food, and cells, easily removed, unlike structured, adherent biofilm.
26
Why does biofilm formation begin at the gingival margin and interdental areas?
These are protected from shear forces and offer favorable niches for bacterial adherence and growth.
27
What role does surface roughness play in biofilm accumulation?
Rough surfaces like restoration margins and implants promote greater bacterial adhesion and retention.
28
What are the main inorganic components of dental calculus?
Calcium phosphate crystals, including hydroxyapatite, octacalcium phosphate, brushite, and whitlockite.
29
What are factors that influence the rate of calculus formation?
Individual variation, tooth location, salivary composition, oral hygiene, and local conditions like inflammation.
30
What is the “reversal phenomenon” in calculus accumulation?
After reaching maximal accumulation (10 weeks–6 months), calculus may decrease due to mechanical wear from food and oral structures.