Exam 3 Flashcards

(106 cards)

1
Q

o Commonly observed in absence of underlying disease state
o May occur due to congenital or developmental reasons

A

Lack of keratinized tissue

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2
Q

What are the periodontal biotypes?

A

Gingival biotype
Bone morphology
Tooth dimension

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3
Q

o Slender, triangular-shaped crown
o Thin, delicate, friable soft tissue with thin alveolar bone
o Narrow zone of keratinized tissue

A

Thin-scalloped gingival biotype

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4
Q

o Slender, triangular-shaped
o Thick, fibrotic gingiva
o Narrow-to-moderate zone of keratinized tissue

A

Thick-scalloped gingival biotype

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5
Q

o Wide, square-shaped crown
o Thick, dense, and fibrotic tissue
o Wide band of keratinized tissue
o Flat gingival margin contour

A

Thick-flat gingival biotype

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6
Q

What is the most common mucogingival deformity?

A

Recession of gingival margin

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7
Q

What contributes to dentin hypersensitivity?

A

Recession of gingival margin

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8
Q

Based on level of gingival margin with respect to mucogingival junction and underlying alveolar bone

A

Miller classification system for gingival recession

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9
Q

Marginal tissue that does not extend to mucogingival junction

A

Miller class I

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10
Q

Marginal tissue recession that extends to or beyond MGJ with no periodontal loss in interdental area

A

Miller class II

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11
Q

Marginal tissue recession that extends to or beyond MGJ with interdental bone or soft-tissue loss and/or malpositioning of teeth

A

Miller class III

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12
Q

Marginal tissue recession that extends beyond MGJ with severe loss of interdental bone to level corresponding to most apical extent of marginal tissue recession

A

Miller class IV

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13
Q

o Uses objective identifiable criterion to classify extent and severity of soft tissue recession
o More reliable; can be used in clinical practice

A

Cairo classification system for gingival recession

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14
Q

 Gingival recession with no loss of interproximal attachments
 Likely due to traumatic brushing

A

Cairo type I

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15
Q

 Gingival recession with loss of interproximal attachment
 Amount of interproximal attachment loss less than or equal to buccal attachment loss
 Associated with horizontal bone loss

A

Cairo type II

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16
Q

 Gingival recession with loss of interproximal attachment
 Amount of interproximal attachment loss greater than buccal attachment loss
 Interproximal defects

A

Cairo type III

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17
Q

What are characteristics of acute periodontal diseases?

A

-Sudden onset
-Rapid progression
-Pain & discomfort
-May be unrelated to preexisting gingivitis/periodon.
-Lesions
-May present with systemic involvement

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18
Q

What is purulence?

A

Pus

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19
Q

Liquification of pus

A

Suppuration

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20
Q

Localized abscess

A

Circumscribed

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21
Q

What do most lesions contain that are predominantly gram-negative and anaerobic?

A

Microflora

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22
Q

constant, localized pain

A

Acute abscess

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23
Q

no pain/dull

A

Chronic abscess

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24
Q

What are the causes of abscesses?

A

-Blocking of orifice of pocket
-Forcing foreign object into tissue
-Incomplete calculus removal in pocket

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25
 Usually, vital pulp  Bone loss present as an angular defect and/or furcation radiolucency  Localized, constant pain
Periodontal abscess
26
 Usually, nonvital pulp  Bone loss at tooth root apex  Difficult to localize, intermittent pain  Inflammatory reaction to pulpal infection or pulpal necrosis  Rapid onset, spontaneous tooth pain, percussion sensitivity, swelling, exudate
Pulpal abscess
27
What are the classifications of abscesses?
Acute Chronic Gingival Periodontal Pericoronal
28
 Rapid onset characterized by pain and discomfort  Primary caused by exacerbation of chronic inflammatory periodontal lesion
Acute abscess
29
 Grows slowing and is not typically painful  Forms after spread of infection controlled by spontaneous drainage, host response, or therapy
Chronic abscess
30
 Primarily limited to gingival margin or interdental papilla without involvement of deeper structures or periodontium
Gingival abscess
31
 Affects deeper structures of periodontium as well as gingival tissue  Usually occurs in site with preexisting periodontal disease including preexisting periodontal pockets
Periodontal abscess
32
 Involves tissues around crown or partially erupted tooth
Pericoronal abscess
33
soft-tissue inflammation associated with abscess
Pericoronitis
34
What are the signs and symptoms of a pericoronal abscess?
o Pain at site o Swelling of perculum o Possible trismus o Elevated body temp o Possible lymphadenopathy
35
What is the management of a pericoronal abscess?
-Establish path of drainage -Thorough instrumentation of affected tooth surface -Pain relief
36
What are the steps in treatment of abscesses?
o Administer local anesthesia o Drain pus o Perform thorough instrumentation o Adjust occlusion and prescribe antibiotics if needed o Recommend warm saline rinses o Prescribe pain medication if needed o Follow up appointment
37
o Localized area of bacterial infection characterized by infection of pulp and periodontal tissues in same tooth o Can originate from dental pulp or periodontal tissue
Endodontic-periodontal lesion
38
What are the signs and symptoms of endodontic-periodontal lesions?
-Deep pockets extending close to root apex -Negative/altered responce to pulp test -Bone resorption in apical/fural region of tooth -Spontaneous pain -Pain on palpitation/percussion
39
 Interdental tissue necrosis  Intense gingival pain  Spontaneous bleeding  Fetid breath  Pseudomembrane formation  Systemic involvement
Necrotizing periodontal disease
40
Noncommunicable, destructive, inflammatory disease o Limited to interdental and marginal gingiva
Necrotizing gingivitis
41
Where is necrotizing gingivitis most commonly found?
Mandibular anterior region
42
What are the characteristics of necrotizing gingivitis?
 Bleeding  Pain  Halitosis  Fever  Lymphadenopathy  Pseudomembrane formation  Ulcers
43
What is the prevalence of necrotizing gingivitis?
Most common in 20-30 years old
44
What are the steps to manage acute necrotizing gingivitis?
1. Management of acute stage 2. Control of preexisting condition 3. Corrective surgical management 4. Maintenance phase
45
o Tissue necrosis spreads to underlying periodontal attachment apparatus o Can lead to bone loss and CAL
Necrotizing periodontitis
46
What is the treatment of necrotizing periodontitis?
 Similar to necrotizing gingivitis treatment  Referral to periodontist recommended  Close collaboration with patient’s medical practitioner
47
o Extension of NG or NP where necrosis progresses to deeper tissues beyond mucogingival line o Symptoms similar to those of NG and NP o Rare, but most extensive and invasive form of NPD o Refer immediately to oral pathologist, oral maxillofacial surgeon, and physician
Necrotizing stomatitis
48
o Caused by herpes simplex virus o Most often HSV-1
Primary herpetic gingivostomatitis
49
 Primarily spread by direct contact  One part of body to another
HSV-1
50
What are the most important stages of primary herpetic gingivostomatitis from a dental management standpoint?
Vesicle & ulcer stage
51
What are clinical signs of primary herpetic gingivostomatitis?
 Oral pain  Swollen/bleeding tissue  Malaise  Swollen lymph nodes
52
What refers to all types of microscopic organisms?
Microbe
53
- Smallest, simplest organisms viewable only through microscope - Most dominant living organisms on planet - Have existed longer than any other life on planet - Reproduce quickly and adapt rapidly
Bacteria
54
Complex multilayered structure that protects microorganism from unpredictable and inhospitable external environment
Bacterial cell envelope
55
Classifies bacteria based on cell envelope structure
Gram staining
56
-Interact with one another -All either gram-pos or gram-neg -Live together in complex microbial communities
Bacteria
57
-Complex, dynamic microbial community embedded within matrix adhered to living or nonliving surface -May be responsible for 65% of diseases
Biofilm
58
-Everywhere in nature -Can exist on any solid surface exposed to microbe-containing fluid -Can be prevalent in natural, industrial, and hospital settings
Biofilm
59
Free-floating microbes attach to surface Timeline?
within minutes
60
Microbes form strongly attached microcolonies Timeline?
Within 2-4 hours
61
Microbes produce initial extracellular matrix Timeline?
Within 6-12 hours
62
Biofilm evolves into fully mature biofilm Timeline?
Within 2-4 days
63
How do mature biofilms protect bacteria?
Blocking Mutual protection Hibernation
64
-Part of normal flora in the mouth -Prevent colonization by opportunistic pathogenic bacteria -Comprise biofilm found on all epithelial-lined surfaces
Commensal bacteria
65
-Relationship with host -Contribute to host nutrition, maintain a robust immune system, and provide cover over mucous membranes -Host provides nutrients, a stable environment for survival
Symbiotic
66
-Microbial imbalance on or inside body -Can result if certain species of microbes become dominant -Occurs when oral biofilm not disrupted frequently -Leads to gingival inflammation
Dysbiosis
67
Triggers inappropriate, excessive host response that results in irreversible periodontal tissue damage
Established dysbiosis
68
What is the most common transmission route of biofilm bacteria? How?
-Vertical -Sharing saliva between caregiver and child
69
What is the less common transmission route of biofilm bacteria? How?
-Horizontal -Same generation kissing
70
What are examples of gram-positive species capable of colonizing in the mouth?
-Streptococcus -Peptostrepococcus -Actinomyces -Rothia -Eubacterium -Mycoplasm
71
What are examples of gram-negative species capable of colonizing in the mouth?
-Neisseria -Veillonella -Aggregatibacter -Campylobacter -Prevotella -Spirochetes of ANUG
72
What are the stages of polymicrobial biofilm formation?
1. inital attachment 2. irreversible attachment 3. maturation I 4. maturation II 5. dispersion
73
-Acquired salivary pellicle immediately forms over clean tooth surface -Free-floating microbes attach using fimbriae -Dynamic and reversible
Step 1: inital attachment of microbes to pellicle
74
-Attained by microbes that can whether hydrodynamic forces and maintain steadfast grip on tooth surface -Microbes begin producing substances that attract other free-floating bacteria to community
Stage 2: Permanent Attachment
75
Microbes begin producing substances that attract other free-floating bacteria to community
coaggregation
76
-Attached bacteria secrete extracellular protective matrix that protects against host immune defenses -Generally consists of proteins, glycolipids, and bacterial DNA
Stage 3: Maturation Phase I: Self-Protective Matrix Formation
77
-Microcolony formation Combination of cell division and recruitment -Microbes cluster, form mushroom-shaped microcolonies that exchange and share nutrients and genetic information -Environmental conditions within microcolonies vary radically, resulting in very diverse population
Stage 4: Maturation Phase II: Mushroom-Shaped Microcolonies
78
Bacteria communicate by releasing and sensing small proteins in a process called
quorum sensing
79
Essential stage of biofilm life cycle
Stage 5: Dispersion
80
Attached to tooth surface; can invade dentinal tubules
Tooth-associated plaque biofilms
81
Adhere to epithelium; can invade gingival tissue
Tissue-associated plaque biofilms
82
Free-floating; not part of biofilm
Unattached bacteria
83
-Activated by immune system in response to offending agent or injury -Traps offending agents or starts healing injured tissue -Not meant to be activated for long time
Inflammatory Response
84
-Network of different types of leukocytes and proteins that work together to defend host from invasion -Necessary for survival
Immune system
85
What are the two divisions of the immune system?
Innate immunity Adaptive (acquired) immunity
86
To defend life of individual (host) by identifying foreign substances in body and defending against them
Primary Purpose of the Immune System
87
The immune system defends life of host by identifying foreign substances in body and defending against them by?
-Deploying immune cells that target invaders -Producing biochemical substances to amplify immune response and counteract foreign invaders
88
Body’s protective response to pathogens, foreign bodies, or injury, characterized by?
-Dilation of blood vessels -Increased permeability of blood capillaries -Increased blood flow -Leukocyte migration into tissues
89
-Short-term process that protects, heals body -Moves plasma and leukocytes into injured tissues
Acute Inflammation
90
What are the classic symptoms of acute inflammation?
Heat Redness Swelling Pain Loss of function
91
Biofilm-induced infection that precipitates complex immunoinflammatory response
Periodontal Disease
92
Mechanisms that enable biofilm bacteria to colonize and damage tissues of periodontium
Virulence factor
93
-Presence of lipopolysaccharide -Ability to invade tissues -Ability to produce enzymes
Primary virulence factors
94
What are the Factors Modulating the Host Immunoinflammatory Response?
Genetic Environmental Acquired
95
What are sent by host cells to activate inflammatory response?
Middlemen
96
What are the Important biochemical mediators?
Cytokines Prostaglandins Matrix metalloproteinases
97
-Powerful regulatory proteins released by host immune cells that influence behavior of other cells -Alert and activate the immune system for help -Can initiate and perpetuate irreversible tissue destruction in chronic inflammatory diseases
Cytokines
98
What are the key cytokines in periodontitis?
IL-1 IL-6 IL-8 TNF-α
99
Powerful biochemical mediators derived from fatty acids expressed on the surface of most cells (D, E, F, G, H, and I)
Prostaglandins
100
What play an important role in bone destruction in periodontitis?
Prostaglandins of E series
101
What trigger osteoclasts to destroy alveolar bone?
Prostaglandins
102
-Family of at least 12 proteolytic enzymes that break down connective tissue matrix -In health, they facilitate the normal turnover of periodontal connective tissue matrix -Released in excessive amounts with intense inflammation
Matrix Metalloproteinases
103
What stimulate leukocytes and fibroblasts to release MMPs?
Cytokines and prostaglandins
104
What can inhibit MMP activity?
Periostat (20-mg doxycycline)
105
In susceptible individuals, dysbiotic biofilm activates host response to produce excessive cytokines, reactive oxygen species, and MMPS, leading to?
Collagen breakdown Bone resorption Periodontal tissue damage
106
What are examples of microscopic organisms?
Bacteria Fungi Protozoa Viruses