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AU14 - Perio Exam 1 > au14_-_periodontology_exam_1_20141210195103 > Flashcards

au14_-_periodontology_exam_1_20141210195103 Flashcards

1
Q

What are 2 other names for the periodontium?

A
  • attachment apparatus- supporting tissues of the tooth
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2
Q

What are the 2 functions of the periodontium?

A
  • attach the tooth to bony tissue of the jaw- maintain integrity of masticatory mucosa
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3
Q

Development of the periodontia occurs early in the ___ phase along with ___ development.

A
  • embryonic phase- tooth development
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4
Q

During periodontia development, cells originate from the ___ and migrate into the ___. These cells form ___ beneath the stomadeal epithelium. The stomadeal epithelium releases factors which initiate ___.

A
  • neural crest- first branchial arch- ectomesenchyme- epithelial-ectomesenchymal interactions
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5
Q

The dental lamina forms what 3 stages?

A
  • bud stage- cap stage- bell stage
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6
Q

During embryogenesis, ectomesenchyme condenses around ___ to form the ___ and the ___.

A
  • dental organ- dental papilla- dental follicle
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7
Q

What does the dental papilla give rise to? What does the dental follicle give rise to?

A
  • gives rise to dentin and pulp- gives rise to periodontium
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8
Q

What does the dental papilla determine?

A

shape and form of the tooth

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9
Q

During embryogenesis, what part of the tooth forms first?

A

crown

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10
Q

During embryogenesis, the outer and inner enamel epithelium proliferate apically to form ___. Odontoblasts form ___. Inner cells secrete ___. The root sheath fenestrates so that ___ cells contact the root surface. ___ induces differentiation of these cells into cementoblast. Cemtnoid forms. Fibers of the cementoid intermingle with immature dentinal fibers.

A
  • Hertwig’s Epithelial Root Sheath- dentin- enamel-related proteins (amelogenins)- ectomesenchymal cells- amelogenin
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11
Q

Periodontal ligament is formed by ___ that are differentiated from the dental follicle lateral to the cementum.

A

fibroblasts

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12
Q

Osteoblasts differentiate from ___.

A

dental follicle ectomesenchymal cells

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13
Q

True or false: Ectomesenchymal cells remain in mature periodontium and participate in turnover.

A

true

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14
Q

What is the definition of gingiva?

A

part of the masticatory mucosa which covers the alveolar process and surrounds the cervical portion of the teeth

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15
Q

What are the 3 parts of the gingiva?

A
  • free gingiva- attached gingiva- interdental papilla
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16
Q

What are other names for free gingiva? It extends from ___ to ___. Is it keratinized?

A
  • gingival sulcus, marginal gingiva, sulcus depth- from free gingival margin to free gingival groove- yes, it is keratinized
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17
Q

Where is the free gingival margin located?

A

on the coronal end of the gingiva, 1.5-2.0 mm coronal to the CEJ

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18
Q

What is the free gingival groove? How prevalent is it?

A
  • junction between free and attached gingiva; corresponds to CEJ- only found in 30-40% of adults
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19
Q

The oral epithelium faces ___. The oral sulcular epithelium faces ___. The junctional epithelium provides contact between ___ and ___.

A
  • oral cavity- tooth surface without contacting it- gingiva and the tooth
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20
Q

What are the macroscopic limits of the free (marginal) gingiva? What are the microscopic limits? Why does it matter?

A
  • extends from FGM to FGG- extends from FGM to JE- because how these landmarks change from health to disease will determine the accuracy of your probe readings
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21
Q

Describe the texture, color, and mobility of attached gingiva. How often is stippling present?

A
  • firm texture- coral pink- immobile- 40% of adults present stippling
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22
Q

How does the width vary in attached gingiva?

A
  • increases with age (passive eruption)- widest in incisors, narrowest in premolars- mandibular lingual: narrowest in incisors, widest in molars
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23
Q

What is the definition of the mucogingival junction? Where is the mucogingival junction not present?

A
  • junction between attached gingiva and alveolar mucosa- not in the palate
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24
Q

True or false: The absence of stippling in the gingiva indicates disease.

A

FALSE: the presence of stippling is an indication of health, but its absence does not mean anything

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25
Q

attached gingiva + marginal gingiva = ___

A

keratinized gingiva

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26
Q

keratinized gingiva - sulcus = ___

A

attached gingiva

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27
Q

What 3 things does the interdental papilla depend upon?

A
  • the contact relationships between adjacent teeth- width of approximal tooth surfaces- course of CEJ
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28
Q

What is the definition of the col? Is it keratinized?

A
  • concavity seen in contact areas of premolar/molar region- non-keratinized epithelium (similar to JE)
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29
Q

The bottom of the gingival sulcus in a healthy mouth is positioned apical to the CEJ. When is this condition most likely to occur?a. prenatallyb. at 10-20 years of agec. before the roots of primary teeth are resorbedd. at 40-60 years of agee. just after a permanent tooth has erupted

A

e. just after a permanent tooth has erupted

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30
Q

Describe the cells of the oral epithelium. Is it keratinized?

A

keratinized, stratified, squamous epithelium (keratinocytes)

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31
Q

What are the 4 layers of the oral epithelium?

A
  • basal layer: stratum basale or stratum germinativum- prickle cell layer: stratum spinosum- granular cell layer: stratum granulosum- keratinized cell layer: stratum corneum
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32
Q

What is the difference between orthokeratinized and parakeratinized?

A
  • orthokeratinized: no nucleus- parakeratinized: nuclear remnants
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33
Q

From the basal layer to the granular layer, do the cytoplasmic tonofilaments increase or decrease? The number of desmosomes? The number of organelles?

A
  • cytoplastmic tonofilaments: increase- desmosomes: increase- organelles: decrease
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34
Q

What are the types of cells in the oral epithelium? What percentage of the cells does each make up?

A
  • keratinocytes (90%)- clear cells: melanocytes, Langerhans cells, Merkel’s cells (10%)
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35
Q

What is the purpose of each of the clear cells in the oral epithelium?

A
  • melanocytes: synthesize melanin pigment- Langerhans cells: defense cells- Merkel’s cells: sensory
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36
Q

Where is the basement membrane? What molecules does it contain?

A
  • present between the basal layer of the oral epithelium and CT; 1-2 micrometers wide- rich in glycoproteins; contains protein-polysaccharide complexes
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37
Q

What are the 2 layers of the basement membrane that are distinguished by electron microscopy? Where is each located?

A
  • lamina lucida: adjacent to basal cells- lamina densa: adjacent to connective tissue; achoring fibers project from LD into CT
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38
Q

What are hemidesmosomes? Desmosomes?

A
  • hemidesmosomes: dense plaques that attach epithelium to the basement membrane- desmosomes: pairs of hemidesmosomes
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39
Q

Describe how stippling is created microscopically.

A
  • at the boundary between the oral epithelium and underlying connective tissue, CT projects into the epithelium papillae- epithelial ridges or rete pegs intervene- when rete pegs fuse and there is no CT support in that area, it is seen as stippling- rete pegs are missing at the JE site
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40
Q

During tooth eruption, the junctional epithelium is derived from ___.

A

reduced dental epithelium

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41
Q

Where is the junctional epithelium the widest?

A

widest in coronal portion (15-20 cell layers) and thin toward the CEJ (3-4 cell layers)

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42
Q

Which has a faster turnover rate: junctional epithelium or oral epithelium?

A

junctional epithelium

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43
Q

Junctional epithelium or oral epithelium?- larger cell size?- larger size of intercellular space?- larger number of desmosomes?- keratinization?

A
  • larger cell size: junctional epithelium- larger size of intercellular space: junctional epithelium- larger number of desmosomes: oral epithelium- JE has potential to keratinize
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44
Q

Where is the JE in comparission to the CEJ in a child? In a healthy adult? In a diseased adult?

A
  • child: JE above CEJ- healthy adult: JE at CEJ- diseased adult: JE below CEJ
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45
Q

Periodontitis occurs when the junctional epithelium ___.

A

migrates apically down the root surface

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46
Q

True or false: Viable junctional epithelium is not necessary for pocket formation.

A

FALSE. It is necessary for pocket formation.

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47
Q

Describe Necrotizing Ulcerative Periodontitis (NUP).

A

junctional epithelium cells die so no pocketing! bone is exposed

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48
Q

What are the cells (6) of the lamina propria and describe what each does?

A
  • fibroblasts: synthesize matrix and fibers- mast cells: vasoactive substances- macrophages: phagocytosis and synthesis- neutrophilic granulocytes- lymphocytes- plasma cells
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49
Q

What are the fibers (4) of the lamina propria and describe each (where they are found, etc.)?

A
  • collagen: characteristic cross-banding; produced by fibroblasts, cementoblasts, and osteoclasts; most abundant- reticulin: numerous adjacent to basement membrane; around blood vessels- oxytalan: mostly in PDL; run parallel to long axis of tooth- elastic: around blood vessels
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50
Q

What are the 3 purposes of the gingival fibers?

A
  • reinforce the gingiva- provide resilience and tone- maintain architectural form and integrity
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51
Q

What are the 4 gingival fibers and where does each run?

A
  • circular fibers: encircle tooth like a cuff- dentogingival fibers: fan out from supra-crestal cementum into free gingiva- dentoperiosteal fibers: run from supracrestal cementum into attached gingiva- trasseptal fibers: run from tooth to tooth (embedded in cementum)
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52
Q

True or false: The periodontal ligament is richly vascular.

A

true

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53
Q

What two structures does the periodontal ligament join?

A

joins cementum and alveolar bone

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54
Q

What are the 2 functions of the periodontal ligament?

A
  • permits forces to be distributed- essential for the tooth mobility
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55
Q

What are the 4 fibers of the periodontal ligament?

A
  • alveolar crest fibers- horizontal fibers- oblique fibers- apical fibers
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56
Q

What are the 6 cells of the periodontal ligament?

A
  • fibroblasts: aligned along principal fibers- osteoblasts: line bone surface- cementoblasts: line cemental surface- osteoclasts: multinucleated; create ruffled surface of bone- epithelial cells- nerve fibers- epithelial cell rests of Mallassez: remnants of the Hertwig’s epithelial root sheath
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57
Q

What is the cementum?

A

mineralized tissue covering root surface and, occassionally, small portions of the crown of the teeth

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58
Q

How is cementum similar to bone? How is it different?

A

DIFFERENT:- no blood vessels- no lymph vessels- no innervation- no physiology resorption/remodelingSIMILAR:- continuing deposition throughout life- collagen fibers embedded in organic matrix- high mineral content (65%), mainly HA

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59
Q

What is the difference between intrinsic and extrinsic cemental fibers?

A
  • intrinsic: produced by cementoblasts; composed of fibers oriented parallel to root- extrinsic: Sharpey’s fibers; produced by PDL fibroblasts
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60
Q

What are the 3 different forms of cemental fibers? Where are each located?

A
  • acellular extrinsic fiber cementum: coronal or middle portion of root- cellular mixed stratified cementum: apical 1/3 of root and in the furcation- cellular intrinsic fiber cementum: resorption lacunae
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61
Q

True or false: Cementum thickness increases by gradual apposition throughout life.

A

true

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62
Q

What is the cementum thickness in the cervical portion of the root? What is the cementum thickness in the apical portion of the root?

A
  • cervical portion: 20-50 micrometers- apical portion: 150-250 micrometers
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63
Q

The alveolar bone consists of ___ bone and ___ bone formed by cells from ___ and ___.

A
  • cancellous- cortical- from the dental follicle- independent of tooth development
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64
Q

What cells/structures are in the bone marrow?

A

adipocytes, vascular structures, and undifferentiated mesenchymal cells

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65
Q

Alveolar bone remodels in response to ___ and ___.

A
  • forces- tooth movement
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66
Q

In the alveolar bone, ___ produce bone matrix (osteoid) consisting of ___, ___, and ___. Osteoid undergoes mineralization by the deposition of minerals like ___.

A
  • osteoblasts- collagen fibers- glycoproteins- proteoglycans- calcium and phosphate
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67
Q

The dental tissue that most closely resembles bone is:a. dentinb. pulpc. cementumd. enamel

A

c. cementum

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68
Q

The supraperiosteal vessels (blood supply to gingiva) are terminal branches of what 7 arteries?

A
  • sublingual artery- buccal artery- mental artery- facial artery- greater palatine artery- infraorbital artery- posterior superior dental artery
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69
Q

What are the 4 arteries that make up the blood supply of the periodontal tissues?

A
  • dental artery- superior/inferior alveolar arteries- intra-septal artery- rami perforantes artery (terminal branch of intra-septal; penetrates alveolar bone all through the socket)
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70
Q

What are the 4 relevant lymph nodes to the periodontia?

A
  • submental lymph nodes- deep cervical lymph nodes- submandibular lymph nodes- jugulodigastric lymph nodes
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71
Q

What are the 7 nerve branches that supply the periodontia?

A
  • infraorbital nerve- sublingual nerve- posterior superior dental nerve- mental nerve- greater palatal nerve- buccal nerve- long sphenopalatine nerve
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72
Q

In health, the periodontal probe penetrates to ___. In disease, the probe penetrates ___.

A
  • free gingival groove- past junctional epithelium into connective tissue
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73
Q

True or false: Diagnosis of periodontitis is based on probe depths.

A

FALSE. It is based on attachment loss, not probe depths.

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74
Q

True or false: The position and dimensions of the contact area determine probe angulations in posterior teeth.

A

true

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75
Q

What is the proper probe angulation and position when charting probe depths?

A
  • find interproximal contact- use contact as guide to insert probe- open angulation by 10 degrees
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76
Q

What was the initial thinking of why gingival recession occurred?

A
  • width of keratinized tissue <2 mm predisposes to recession- narrow gingiva cannot protect from friction and cannot buffer against muscle pull- facilitates subgingival plaque formation since mobile tissue causes pocket to open, facilitates food impaction, and impedes oral hygiene
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77
Q

What is the current thinking of how gingival health is related to the width of the gingiva?

A
  • gingival health can be maintained independent of its dimensions- narrow gingiva has same resistance to attachment loss as wide gingiva
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78
Q

The thin phenotype has:___ (inc/dec) recession___ (more/less) vulnerable to trauma___ (more/less) inflammation___ (more/less) favorable treatment outcome (root coverage, GTR, etc.)

A
  • increased recession- more vulnerable- more inflammation- less favorable
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79
Q

When would you recommend gingival grafts?

A
  • when recession causes symptoms (caries, esthetic concerns, progressive recession, sensitivity)- subgingival restoration margins on thin biotype- pre-orthodontic therapy (final tooth position will be buccal)
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80
Q

Are the characteristics of the gingiva determined by genetics or by functional adaptation to environmental stimuli?

A

genetics

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81
Q

The initial thought was that gingiva will become keratinized in response to friction, but now we think ___.

A

connective tissue determines epithelial characteristics

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82
Q

Early grafting procedures involved ___ and ___ with the rationale that ___.

A
  • free gingival grafts- coronally advanced flaps- keratinized epithelium converted to firm attached gingiva
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83
Q

What type of gingival graft is now used? With what rationale?

A
  • connective tissue graft- connective tissue determines epithelial prototype
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84
Q

What are the 2 parts of the soft tissue attachment to the tooth? How large is each? How does this relate to the biologic width?

A
  • fibrous connective tissue (1.06-1.08 mm)- junctional epithelium (1.4 mm)- approx 1 mm of free gingiva which allows for a 3 mm total biologic width
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85
Q

The distance from the CEJ to the alveolar crest is ___. The distance from crown margins to alveolar crest has to be ___. If you don’t have this distance, then ___.

A
  • 3 mm- 3 mm- crown lengthening
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86
Q

Describe the process of healing after a tooth extraction.

A
  • clot formation- wound cleansing PMNs, monocytes, macrophages migrate into the wound- new vasculature, mesenchymal cells (from PDL) form granulation tissue- provisional connective tissue- immature bone forms- bundle bone (socket proper) is resorbed- wound filled with woven bone- bone maturation
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87
Q

True or false: Socket preservation is important for preserving bone morphology.

A

true

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88
Q

What is guided tissue regeneration? How is this clinically applied?

A
  • epithelium grows faster than bone or connective tissue; epithelial exclusion will allow selective growth of these cells- use barrier membranes
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89
Q

How were studies on plaque formation conducted?

A
  • adhesive tape samples from the tooth surface- plaque grown on epoxy resin crowns worn for different time periods- in vitro studies of attachment and aggregation between different bacterial species- experimental gingivitis models
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90
Q

Early studies of oral microbiology were based on: ___ and ___.

A

cultivation and microscopy

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91
Q

What is the great plate anomaly?

A

when you look under a microscope, you see 100 species, but on a plate, only 50 grows; not everything you see will grow

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92
Q

What is the “we know what we can grow” bias?

A

all studies focused on cultivable species, but there are so many more species in the mouth

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93
Q

What approaches to study oral microbiolgy revolutionized species identification?

A

molecular (DNA, RNA) approaches

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94
Q

How many distinct oral species are there? What % have never been cultured?

A
  • more than 700 distinct oral species- +60% never have been cultured- includes exotics (ex. Archea) like termite guts and other extreme environments- fungi and viruses may also play a role in disease
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95
Q

What is the definition of a plaque biofilm?

A

organized cooperating community of organisms with specific inter-bacterial and host-bacterial interactions

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96
Q

What is atopic dermatitis?

A

“Purell disease”; children who are not exposed to bacteria when they are young begin making autoantibodies; 1st world problem (seriously!)

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97
Q

In the attachment stage of biofilm formation, planktonic bacteria adhere to ___ which is made up of ___ and ___. There is an alteration in ___ and ___.

A
  • acquired pellicle- salivary glycoproteins- antibodies- surface charge- free energy
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98
Q

What is the difference between rapid attachers and slow attachers?

A
  • rapid attachers: specific attachment structures (fimbrae, extracellular polymers, glycocalyx)- no specific mechanism
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99
Q

How do bacterial characteristics change following attachment?

A
  • synthesis of new outer membrane proteins- active cellular growth
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100
Q

What is the difference between co-aggregation and co-adhesion during the growth phase of biofilm formation?

A
  • co-aggregation: cell-to-cell recognition of genetically distinct cell types; mediatedby protein or glycoprotein receptors on one cell and carbohydrates on the other; all cells are suspended; “clumps” form which then attach to the pellicle- co-adhesion: interactions between suspended and already adhering microorganisms; influenced by temperature and lactose
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101
Q

What two factors affect co-adhesion?

A
  • temperature: no co-adhesion at higher than 37 degrees- lactose: inc lactose, dec co-adhesion
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102
Q

What 3 things occur during biofilm maturation?

A
  • increase in diversity- replication and matrix formation- ecological succession
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103
Q

What are the 3 categories of bacteria in ecological succession?

A
  • tertiary colonizers: gram negative- secondary colonizers: bridge species- primary colonizers: gram positive and some negative
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104
Q

Which bacterial colonizers are usually beneficial? Which are usually pathogenic?

A
  • beneficial: primary colonizers- pathogenic: tertiary colonizers
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105
Q

Name examples of tertiary, secondary, and primary colonizers.

A
  • tertiary: Porphyromonas gingivalis, A. actinomycetemcomitans- secondary: F. nucleatum- primary: S. sanguis
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106
Q

S. sanguis is found in large numbers in deep, active periodontal pockets. Through scaling and root planing of a deep periodontal pocket will most likely result in increased numbers of A. actinomycetemcomitans.State whether each statement is true or false.

A

both are false

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107
Q

When a biofilm increases in thickness, what changes?

A
  • difficulty in diffusion in and out of the biofilm- an oxygen gradient develops- completely anaerobic (no oxygen) conditions emerge in the deeper layers- reverse gradients of fermentation products develop as a result of bacterial metabolism
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108
Q

How does the nutrition in the biofilm differ between the supragingival plaque and subgingival plaque?

A
  • supragingival plaque: dietary products dissolved in saliva- subgingival plaque: periodontal tissues and blood (“clavicular fluid”); bacterial hydrolytic enzymes breakdown host macromolecules into peptides and amino acids
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109
Q

What makes up 15-20% of a biofilm? What makes up the remaining biofilm?

A
  • microcolonies (15-20%)- interbacterial matrix
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110
Q

What are the 3 sources of the biofilm matrix?

A
  • dead bacterial cells- saliva- gingival exudate
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111
Q

Are there voids/water channels in a bacterial biofilm? What makes up the backbone of the biofilm?

A
  • yes- exopolysaccharides
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112
Q

Compare the lower layer, loose layer, and fluid layer of the biofilm.

A
  • lower layer: dense microbes, polysaccharide matrix, tightly bound together, steep diffusion gradients- loose layer: irregular in appearance, extends into surrounding media- fluid layer: stationary sublayer, fluid layer in motion, nourishes the biofilm by molecular diffusion
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113
Q

Do shear forces determine the colony shape in supra or subgingival plaque? What do colonies with low shear force look like? With high shear force?

A
  • supragingival plaque- low shear force: towers or mushrooms- high shear force: elongated colonies capable of oscillation (like seaweed)
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114
Q

Describe the difference between a gram-positive matrix and gram-negative matrix.

A
  • gram-positive: very fibrillar, due to dextrans and levans- gram-negative: very regular; contains tri-laminar vesicles; filled with endotoxins and proteolytic enzymes; probably involved in adherence
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115
Q

Describe the structure of subgingival plaque.

A
  • cuticle forms primary attachment- structure similar to supragingival plaque- bacterial layers near sulcular epithelium different from tooth-attached (no inter-bacterial matrix, more spirochetes and flagellated bacteria)
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116
Q

What are the 3 bacteria mentioned as an example of bacterial collaboration? How do they collaborate?

A
  • Streptococcus cristatus: 1st colonizer; facultative species (can live with or without O2); uses up O2 when available- Fusobacterium nucleatum: 2nd colonizer; robust anaeriobe; binding to Strep improves survival when O2 is present- Porphyromonas gingivalis: 3rd colonizer; microaerophilic, obligate anaerobe; coagregation essential to survival when O2 is present
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117
Q

How did F. nucleatum and S. cristatus interact during the tissue culture experiment?

A
  • F. nucleatum invades epithelial cells- S. cristatus does not invade cells- after coaggregation, S. cristatus is carried inside by F. nucleatum
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118
Q

What are the advantages to biofilm living?

A
  • DEFENSE: presence of concentrated bacterial enzymes; inter-bacterial matrix- PROTECTION FROM EXTERNAL CHANGES: diffusion minimal in interior regions; antibiotic and antimicrobial resistance; protection from friction and shearing forces; attachment- TRANSFER OF INFORMATION AND GENETIC MATERIAL: signaling (quorum sensing); conjugation; transformation; plasmid transfer; trasposon transfer
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119
Q

What is the definition of quorum sensing?

A

regulation of expression of specific genes through accumulation of signaling compounds that mediate intercellular communication

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120
Q

Describe the process of quorum sensing between commensal and pathogenic bacteria.

A
  • auto-inducer (AI) 1 or 2 turns on in response to cell density- commensal bacteria produce and respond to low levels of AI-2- pathogens produce AI-2 in high levels- Al-2 may determine the switch from commensal to pathogenic community
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121
Q

What are the 3 reasons why biofilm bacteria are more resistant to antibiotics?

A
  • BIOFILM BACTERIA GROW MORE SLOWLY (antibiotics depend on cell turnover for efficacy; slow-growers express “non-specific defense mechanisms”; slow growers make more exo-polymers)- EXO-POLYMERS RETARD DIFFUSION (ion-exchange mechanism prevents highly charged molecules from reaching deeper zones; extracellular enzymes inactivate antibiotics)- BIOFILM BACTERIA EXPRESS DIFFERENT GENES (gene transfer; phenotypic expression of biofilm existence)
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122
Q

Why don’t oral pathogens fit the usual model of a pathogen?

A
  • oral pathogens are normally present throughout life- damage requires presence in large numbers
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123
Q

The ecological concept of oral microbial diseases states…

A
  • ecological shifts lead to changes in proportions- balance shifts in favor of “pathogens”/disease- periodontal disease is an example of “ecological catastrophe”
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124
Q

Which of the following is NOT a reason why growth of a microbe is different in nature compared to pure culture?a. limited nutrients in natural environmentb. poor nutrient distribution in natural environmentsc. not optimal temperature in natural environmentsd. lack of competition in natural environments

A

d. lack of competition in natural environments

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125
Q

What is the clinical significance (3) of biofilm formation?

A
  • tooth-brushing has an effect on where the biofilm is located (interproximal, fissures, etc.) and non-contact brushing can remove towers and mushrooms by shear forces- antibiotic resistance- translocation and transmission of bacteria
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126
Q

What are the 2 targets of therapy in the prevention of biofilms?

A
  • AI-2- vaccines that target common resistance genes
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127
Q

What are the different ways bacteria can translocate in the mouth?

A
  • periodontal probe can translocate pathogens from pockets to healthy sites- drug-resistant strains can translocate to neighboring teeth- teeth act as reservoirs for colonization of implants- bacteria can infect membranes in GTR
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128
Q

What is Leuven’s “one-stage full-mouth disinfection”?

A
  • full-mouth scaling and root-planing within 24 hours- subgingival irrigation with 1% chlorhexedine- tongue brushing- oral antimicrobial rinse
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129
Q

True or false: Plaque cannot form on implant abutments.

A

FALSE; plaque can form on implant abutments

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130
Q

Implants that fail have a microbial composition similar to ___.

A

periodontal disease

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131
Q

What is the non-specific plaque hypothesis?

A
  • plaque control important in periodontal treatment- all plaque bacteria considered bad- any accumulation of micro-organisms at or below the gingival margin causes inflammation
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132
Q

What is the specific plaque hypothesis?

A
  • specific organisms in dental plaque are the etiological agents- microbial composition of disease sites different from healthy sites- local debridement and systemic antibioitcs could control LAP
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133
Q

What are the prerequisites for disease initiation and progression?

A
  • VIRULENT PERIODONTAL PATHOGEN: P. gingivalis with type II and IV fimA genotypes; virulence factors; right location in the site (adjacent to epithelium, apical part of the pocket)- LOCAL ENVIRONMENT: colonization by beneficial species dilutes and inhibits pathogens; effect of local “regulon”/subgingival environment (iron increases outer membrane protein expression in P. gingivalis and S. cristatus can inhibit fimA expression)- HOST SUSCEPTIBILITY: HIV infection; diabetes; smoking
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134
Q

What are the 4 different ways through which pathogens colonize?

A
  • ADHESINS ON BACTERIA BIND HOST RECEPTORS: type I or IV collagen, sialic acid, galactosyl residues; bacteria have fimbriae or outer membrane proteins- COAGGREGATION- NUTRIENT UTILIZATION: Veillonella uses lactate made by streptococci; Campylobacter uses formate made by Selenomonas; Porphyromonas uses hermin from blood in sulcus- COMPETITIVE INHIBITION: bacteriocins; hydrogen perioxide production
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135
Q

What are the 3 ways through which pathogens overcome host defenses?

A
  • DESQUAMATION OF EPITHELIUM: invade epithelium and bind to underlying cells- PREVENT ANTIBODY-BINDING: IgG and IgA proteases; mimic host antigens- PREVENT PHAGOCYTIC CELLS: leukotoxin; non-lethal suppression of immune cells
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136
Q

The World Workshop in 1996 designated 3 pathogens. What are they?

A
  • P. gingivalis- A. actinomycetemcomitans- T. forsythia
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137
Q

Is Actinobacillus actinomycetemcomitans (AA) motile? Gram positive or negative? How does it get its energy? Aerobic or anaerobic? Shape of bacteria and colonies?

A
  • non-motile- gram-negative- saccharolytic (breaks down carbs for energy)- capnophlic (thrive in high CO2)- round-ended rod; star-shaped colonies
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138
Q

What is the evidence of AA as a pathogen based on association?

A
  • high numbers associated with agressive periodontisis- detected in active sites- detected in prospective studies
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139
Q

What is the evidence of AA as a pathogen based on elimination?

A
  • elimination or suppression resulted in successful therapy- recurrent lesions harbor the species
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140
Q

What is the evidence of AA as a pathogen based on host response? It also inhibits ___ and induces ___.

A
  • high levels of systemic and local antibody response- inhibits growth of commensals (S. sanguis)- induces disease in animal models
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141
Q

What is the evidence of AA as a pathogen based on virulence factors?

A
  • tissue invasive (epithelial and endothelial cells)- leukotoxin- fibroblast inhibiting factor- endotoxin- collagenase
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142
Q

What is the evidence AGAINST AA being a pathogen?

A
  • not seen in all cases of aggressive periodontitis- seen in periodontally healthy subjects- genetic analysis of the leukotoxin gene (13 clusters identified; II seen in severe disease; XII and XIV associated with health)- AA with 530 bp deletion is 23x more likely to be disease-associated than AA with full length promoter region
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143
Q

There are ___ serotypes of AA which are based on ___. ___ are the dominant antigens.

A
  • 5- polysaccharides on the surface of an organism- serotype-specific surface antigens (SPA)
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144
Q

Serotype ___ of AA is most commonly associated with localized aggressive periodontitis in the USA. It has a role in resistance to ___.

A
  • b- resistance to phagocytosis and killing by PMNs
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145
Q

Serotype ___ of AA is health-associated in Finland and disease-associated in Japan.

A

a

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146
Q

For an AA infection, ___ and ___ approach is vital to treatment. ___ and ___ are effective in reducing bacterial load. ___ approach is required to eliminate tissue reservoirs.

A
  • mechanical- chemotherapeutic- amoxicillin 500 mg- metronidazole 250 mg- surgical
147
Q

Which of the following is not a virulence factor produced by A. actinomycetemcomitans?a. leukotoxinb. collagenasec. lipoteichoic acidd. lipopolysaccharide

A

c. lipoteichoic acid

148
Q

Is Porphyromonas gingivalis gram positive or negative? Aerobic or anaerobic? Motile? What is the shape of the bacteria and the color of the colonies?

A
  • gram-negative- anaerobic- non-motile- asacharolytic rods; black pigmented Bacteriodes
149
Q

What is produced by PG?

A
  • collagenase- proteases- hemolysins- endotoxin- fatty acids- NH3- H2S- indole
150
Q

For PG, what are cysteine proteases important for?

A
  • protein degradation- the maturation of cell surface proteins such as fimA fimbrillin
151
Q

What is the evidence (4) of PG as a pathogen based on association?

A
  • elevated in lesions of periodontitis- lower in healthy sites and subjects- elevated in progressing lesions- presence indicates increased risk for attachment loss
152
Q

What is the evidence (3) of PG as a pathogen based on elimination?

A
  • elimination results in successful therapy- recurrent lesion harbor organisms- successful therapy lowered antibody level
153
Q

What is the evidence of PG as a pathogen based on host response?

A

elevated antibody in serum/saliva of subjects with periodontisis

154
Q

What is the evidence of PG as a pathogen based on virulence factors?

A
  • several factors- invades epithelial cells in vitro
155
Q

What is the evidence of PG as a pathogen based on animal studies?

A
  • induces disease in gnotobiotic rats- immunization decreased disease in animals
156
Q

What is the evidence AGAINST PG as a pathogen?

A
  • seen in health- not always seen in disease- high antibody response- not numerous in the subgingival community
157
Q

Is Tannerella forsynthia gram positive or negative? Aerobic or anaerobic? What is the shape of the bacteria?

A
  • gram-negative- anaerobic- spindle shaped; highly pleomorphic rod
158
Q

What does TF require? With what bacteria does it co-cultivate? What is on its cell surface and what does that do?

A
  • requires N-acetylmuramic acid (NAM)- co-cultivates with F. nucleatum- serrated S-layer on cell surface (mediates adhesion and hemagglutination)
159
Q

What is the evidence of TF as a pathogen based on association?

A
  • elevated in lesions of periodontitis- lower in healthy sites and subjects- elevated in progressing lesions- presence indicates increased risk of attachment loss
160
Q

What is the evidence of TF as a pathogen based on elimination?

A
  • elimination results in successful therapy- recurrent lesion harbor organism- reduced in successfully treated peri-implants
161
Q

What is the evidence of TF as a pathogen based on host response?

A

elevated antibody in serum/saliva of subjects with refractory periodontitis

162
Q

What is the evidence of TF as a pathogen based on virulence factors?

A
  • several factors- invades epithelial cells in vitro
163
Q

What is the evidence of TF as a pathogen based on animal studies?

A

induces disease in gnotobiotic rats

164
Q

Is Spirochetes gram negative or positive? Aerobic or anaerobic? What shape is the bacteria? Are they motile?

A
  • gram-negative- anaerobic- helical-shaped- highly motile organisms
165
Q

Is Prevotella intermedia/nigrescens gram positive or negative? What is the shape of the bacteria and the appearance of the colonies? Aerobic or anaerobic?

A
  • gram-negative- short, round-ended rod; black pigmented Bacteriodes- anaerobic
166
Q

Prevotella intermedia/nigrescens has luxuriant growth in ___. It is associated with what types of gingivitis? It is elevated in ___.

A
  • naphthoquinone- puberty/pregnancy gingivitis- NUG
167
Q

What is the evidence for P. intermedia/nigrescens as a pathogen?

A
  • seen in progressing sites- demonstrated in intercellular spaces- induces alveolar bone loss in rats- sites with Pi/Pn show persistent BOP- amox + metro decreases BOP and Pi/Pn levels- releases MMP-8 and -9 in pockets
168
Q

Fusobacterium nucleatum is gram positive or negative? Aerobic or anaerobic? What shape is the bacteria? What is this bacteria’s role?

A
  • gram-negative- anaerobic- spindle-shaped rod- early colonizer in plaque; bridging organism
169
Q

Is FN found supra or subgingival? It can induce ___. What does it release?

A
  • subgingival microbiota in health and disease- induce cell death in leukocytes- releases cytokines, elastase and oxygen radicals from leukocytes
170
Q

The organism that is found MOST often in both remission and progression of adult periodontitis is:a. Eubacterium timidumb. Tannerella forsythiac. Prevotella intermediad. Fusobacterium nucleatum

A

d. Fusobacterium nucleatum

171
Q

How many oral species are present? What % are uncultivated?

A
  • 700 oral species- 60-80%
172
Q

What is the definition of dental calculus?

A

mineralized plaque that forms on the surfaces of natural teeth and dental prostheses

173
Q

What are the 2 types of dental calculus? What is the difference between the two?

A

SUPRAGINGIVAL:- coronal to gingival margin- white or white/yellow- clay-like consistency- easily detached from tooth surface- commonly found opposite salivary ductsSUBGINGIVAL:- below the gingival margin- hard, dense- dark-colored- extends to the base of pocket but does not reach JE* with gingival recession, subgingival can become supragingival

174
Q

What are the 4 ways to detect dental calculus?

A
  • tactile exploration- dental radiographs (not always) (detection of spurs)- a blast of air to open gingival margins- color of the overlying gingiva
175
Q

True or false: Calculus is the primary cause of periodontitis.

A

FALSE. Calculus represents a secondary product of infection and is NOT a primary cause of periodontitis.

176
Q

Clinically, subgingival calculus is the most frequently diagnosed using which one of the following methods:a. a 5-second blast of airb. a periapical x-rayc. an MRId. tactile exploratione. disclosing with erythrosine solution

A

d. tactile exploration

177
Q

What are the 2 ways calculus attaches to the tooth?

A
  • UNDERLYING PELLICLE: pelllicle calcifies and attaches to cementum, enamel, or dentin- PENETRATION OF SURFACE IRREGULARITIES: caries, exposed root cementum, previous insertion of Sharpey’s fibers, and root resorption
178
Q

The mineralization of calculus begins in ___.

A

the bacterial colonies or ECM

179
Q

What are the 4 forms of calcium phosphate?

A
  • CaH(PO4) x 2H2O = brushite (B)- Ca4H(PO4)3 x 2H2O = octa calcium phosphate (OCP)- Ca5(PO4)3 x OH = hydroxyapatite (HA)- beta-Ca3(PO4)2 = whitlockite (W)
180
Q

Which form of calcium phosphate is the basis for supragingival calculus formation and seen in recent (<2 weeks old) calculus?

A

CaH(PO4) x 2H2O = brushite (B)

181
Q

Which form of calcium phosphate is predominant in exterior layers and forms platelet like crystals?

A

Ca4H(PO4)3 x 2H2O = octa calcium phosphate (OCP)

182
Q

Which form of calcium phosphate is predominant in inner layers of old calculus and forms rod or sand-grain-like crystals?

A

Ca5(PO4)3 x OH = hydroxyapatite (HA)

183
Q

Which form of calcium phosphate is most common form in subgingival calculus and has hexagonal crystals?

A

beta-Ca3(PO4)2 = whitlockite (W)

184
Q

True or false: Calculus is covered by a layer of viable plaque.

A

true

185
Q

True or false: The roughness of calculus initiates gingivitis.

A

FALSE. The roughness of calculus does NOT initiate gingivitis.

186
Q

True or false: Calculs impedes oral hygiene measures.

A

true

187
Q

True or false: Calculus keeps plaque in close proximity to tissues.

A

true

188
Q

True or false: Calculus is removed due to its plaque retentive nature.

A

true

189
Q

How do bacteria induce damage to periodontal tissues?

A
  • bacteria attach and colonize the gingival crevice; some species can invade periodontal soft tissue- bacteria release substances that directly damage host cells- bacteria activate the host’s own inflammatory and immune systems, leading to host tissue damage
190
Q

What are the (4) major microbial virulence factors?

A
  • ability to invade periodontal epithelium- direct cytotoxic effects of bacterial metabolic waste products (ammonia, intole compounds, fatty acids, hydrogen sulfide)- damaging bacterial enzymes (leukotoxin, gingipains)- immunostimulatory molecules (LPS from gram-negative, lipoteichoic acids from gram-positive, gingipains, formylpeptides, other surface antigens)
191
Q

What are the (3) mechanisms of periodontal defense?

A
  • prevention of bacterial entry (passive protection by periodontal epithelium)- innate immune responses (non-specific, first line of active defense)- acquired (adaptive) immune responses (specific, second line of active defense)
192
Q

What are the (3) ways to prevent bacterial entry?

A
  • shedding of epithelial cells into the oral cavity (inhibits bacterial colonization of mucosa)- intact epithelial barrier- positive fluid flow into the gingival crevice
193
Q

Gingival crevicular fluid originates as ___.

A

gingival tissue interstitial fluid

194
Q

What are the 4 effects of the complement system?

A
  • induces bacterial lysis- promotes phagocyte recruitment (chemotaxis)- promotes phagocytosis by opsonization of bacteria- helps activate mast cells, which increases vascular permeability
195
Q

During the innate immune response, oral mucosa produces ___ and the oral epithelium produces ___.

A
  • antimicrobial peptides- pro-inflammatory cytokines
196
Q

___ and ___ are universal signals of infection that help recruit inflammatory cells. ___ attracts neutrophils in the early stages of infection.

A
  • IL-1beta- TNF-alpha- IL-8
197
Q

The innate immune response has the antimicrobial effect of ___, ___, and ___ as well as the phagocytic effects of ___ and ___.

A
  • antibodies- lactoferrin- lysozyme- neutrophils- macrophages
198
Q

___, ___, and ___ are hallmarks of adaptive immunity.

A
  • antigen recognition- immune memory- clonal expansion
199
Q

Serum complement and neutrophils cause ___. Monocytes and macrophages and lymphocytes cause ___.

A
  • acute inflammation resolution- chronic inflammation resolution
200
Q

What are the (5) reservoirs of supragingival bacteria?

A
  • tongue- oral mucosa- tonsils- saliva- supragingival plaque
201
Q

What are the (4) reservoirs of subgingival bacteria?

A
  • periodontal soft tissues- dentinal tubules- furcations- subgingival calculus
202
Q

___ plays a major role in defense of the oral cavity.

A

innate immunity

203
Q

Toll-like receptors (TLRs) have a major role in ___. They recognize ___.

A
  • induction of innate immune response- conserved microbial-associated molecular patterns (including LPS, lipoteichoic acid and flagellas)
204
Q

What cells express toll-like receptors?

A

all cells, including epithelial cells, PMNs, monocytes, and macrophages

205
Q

TLRs signal for cells to produce ___, ___, ___, ___, and ___.

A
  • cytokines- chemokines- antimicrobial peptides- nitric oxide- eicosanoids
206
Q

What are the (8) biological activities of LPS (endotoxin)?

A
  • complement activation- PMN activation- macrophage activation- B-cell mitogen activity- pyrogenicity- stimulation of bone resorption- stimulation of prostaglandin synthesis- induction of Tumor Necrosis Factor (TNF-alpha)
207
Q

What are the 2 pathways of the complement system?

A
  • classical pathway- alternative pathway
208
Q

What cytokines are involved in pro-inflammatory activity?

A

IL-1beta, TNF-alpha

209
Q

What cytokine is used for chemotactic activity?

A

IL-8

210
Q

Prostaglandins are derived from ___ and produced by ___ and other cells.

A
  • arachidonic acid- activated macrophages
211
Q

What do prostaglandins induce, especially PGE2?

A
  • vasodilation - cytokine production- production of matrix metalloproteinases by fibroblasts and osteoclasts which damage periodontal tissues
212
Q

What do matrix metalloproteinases do? Where are the concentrations the highest? Name an example of a metalloproteinase.

A
  • degrade extracellular matrix- concentrations are higher in inflamed gingiva than in healthy gingiva- PMN collagenase (degrades the major structural protein in gingiva)
213
Q

What does proteinase inhibitors do? What are 2 examples and what does each example do?

A
  • antagonize inflammation; inhibit degradation of matrix proteins- alpha-2 macroglobulin: broad spectrum proteinase inhibitor- alpha-1 antitrypsin: broad spectrum proteinase inhibitor and potent inhibitor of PMN collagenase
214
Q

What are the 2 types of antimicrobial peptides discussed in lecture? What does each do? Where is each produced?

A
  • DEFENSINS: inhibit bacteria and fungi; produced by salivary gland epithelium- CALPROTECTIN: inhibits bacteria and fungi by chelating zinc; produced by epithelium, PMNs, monocytes, and macrophages
215
Q

Neutrophils are deployed from ___. Macrophages are found in ___. Mast cells are found ___, especially ___.

A
  • blood- organs and tissues- throughout the body- connective tissue subjacent to mucosal surface
216
Q

Acute inflammation or injury increases ___, resulting in ___, ___, and ___.

A
  • vascular permeability- redness- edema- increased gingival crevicular fluid flow
217
Q

PMN deliver ___ to bacteria in the ___ stages of infection.

A
  • antimicrobial substances- early
218
Q

True or false: PMNs kill only by oxidative mechanisms.

A

FALSE. PMNs kill by oxidative and non-oxidative mechanisms.

219
Q

PMN activities are triggered by ___. PMN surface has many ___.

A
  • receptor binding events- high affinity receptors
220
Q

Describe the process of PMN recruitment to the gingival crevice.

A
  • LPS proteases- release of proinflammatory cytokines (IL-1, TNF)- endothelial cells increase their adhesion molecule expression (CAM-1, ELAM-1)- neutrophil-endothelial cell binding occurs and migration begins- neutrophils follow chemotactic gradient through the junctional epithelium into the crevice
221
Q

What are the steps in PMN extravasation?

A
  • random contact- rolling- sticking- extravasation
222
Q

Rank the numbers of T lymphocytes, B lymphocytes, and plasma cells from most to least in chronic periodontitis.

A

plasma cells > B lymphocytes > T lymphocytes

223
Q

In the adaptive immune response, ___ and ___ function as antigen presenting cells.

A
  • macrophages- Langerhans cells
224
Q

The T-cell receptor has 2 ___ chains (alpha and beta). The variable segments determine ___.

A
  • glycoprotein- the type of immune response
225
Q

True or false: TCR are different between chronic and aggressive periodontitis.

A

true

226
Q

What are the cytokines associated with Th1 cells? With Th2 cells? What cytokine is associated with both?

A
  • Th1: IL-2, IFN-gamma, TNF-alpha- Th2: IL-4, 5, 6, 10, 13- IL-10
227
Q

Which helper T-cell has to do with cell-mediated immunity? Which has to do with antibody production?

A
  • Th1- Th2
228
Q

Cytotoxic T-cells are activated by ___. Tc cells respond to ___. Antigens from these pathogens bind ___.

A
  • cytokines- intracellular pathogens- MHC I molecules
229
Q

True or false: Tc cells are found in high numbers in periodontitis.

A

FALSE. Not many Tc cells are found in periodontitis, suggesting that viruses and invasive bacteria are not major players.

230
Q

Humoral immunity is triggered in response to ___. Antigen-antibody complex activates ___ and facilitates ___. Th2 cytokines activate ___.

A
  • soluble antigens- complement- opsonization- B cells to plasma cells
231
Q

What are the 2 types of B cells? What does each do? Do their levels ever decrease?

A
  • CONVENTIONAL: produce antibodies against bacteria; levels decrease in healthy and treated sites- AUTOREACTIVE: produce auto-antibodies; levels do not decrease after treatment
232
Q

What antibodies are prevalent in the primary response? In the secondary response?

A
  • primary: IgM (first) and then IgG- secondary: IgG (predominantly) and a little IgM
233
Q

What are the mechanisms of antibodies acting alone? Antibody plus complement? Antibody plus cells?

A
  • ANTIBODY ALONE: block entry of toxins and viruses; immobilizes bacteria; agglutinates bacteria- ANTIBODY PLUS COMPLEMENT: lyses bacteria- ANTIBODY PLUS CELLS: opsonizes bacteria and fungi for phagocytosis; activates extracellular killing
234
Q

True or false: The avidity, or antigen binding, differs among antibody subclasses. Not all are capable of effective opsonization or complement activation.

A

true

235
Q

Which antibody, IgG1 or IgG2, is more prevalent in chronic periodontitis? In aggressive periodontitis?

A
  • chronic: IgG1- aggressive: IgG2
236
Q

IgG2 recognizes ___ while other subclasses mainly recognize ___.

A
  • carbohydrate antigens (LPS)- protein antigens
237
Q

Describe the steps of a systemic humoral immune response to plaque antigens in the gingival crevice.

A
  • plaque antigens diffuse through the JE- Langerhans cells within the epithelium capture and process the antigens- antigen-presenting cells (macrophages and Langerhans) leave the gingiva in the lymph- antigen-presenting cells reach the lymph node and begin to stimulate lymphocytes to produce a specific immune response- periodontal microbe specific antibodies are produced by plasma cells within the lymph nodes and travel back to the gingiva via blood vessels- antibodies leave the circulation and are carried to the crevice in the transudate from the inflamed and dilated blood vessels- antibody action on microbes in the crevice can result in killing, aggregation, precipitation, detoxification, opsonization, and phagocytosis of bacteria
238
Q

Describe the steps of a local cellular immune response to plaque antigens in the gingival crevice.

A
  • plaque antigens diffuse through the JE- Langerhans cells within the epithelium capture and process the antigens- antigen-presenting cells (macrophages and Langerhans) leave the gingiva in the lymph- antigen-presenting cells reach the lymph node and begin to stimulate lymphocytes to produce a specific immune response- periodontally specific B cells and T cells proliferate within the lymph nodes and enter the blood- periodontally-specific lymphocytes “home” back to the periodontium and locate within the tissues where they begin their humoral and cell-mediated immune functions- antibodies are produced locally by plasma cells which are controlled by Th2 cells; cell-mediated immune activity is regulated by Th1 helper cells
239
Q

Homing of relevant immune cells takes place ___.

A

within the periodontal lesion

240
Q

Which Th cells are more prevalent in chronic periodontal lesions?

A

Th2

241
Q

Which cells are among the most predominant active secretory cells in advanced periodontal lesions?

A

plasma cells

242
Q

True or false: The ratio of IgG subclasses are similar in serum and gingival crevicular fluid.

A

true

243
Q

True or false: An individual’s ability to mount a specific antibody response to bacteria in the subgingival biofilm may indicate a patient’s susceptibility to the disease and ability to respond to treatment.

A

true

244
Q

You can diagnose active periodontitis by screening ___ or screening ___.

A
  • whole saliva- gingival crevicular fluid
245
Q

In healthy gingiva, the tissue volume ratios are: ___% JE, ___% OE, and ___% CT.

A
  • 10% JE- 30% OE- 60% CT
246
Q

In healthy gingiva, the JE is how many cell layers thick?

A

10-20 cell layers

247
Q

What is the name of capillary loops in healthy gingiva? Are the number of loops constant?

A
  • subepithelial plexus- yes, it is constant
248
Q

The subepithelial plexus contains anastomoses of ___ blood vessels with vessels from ___.

A
  • supraperiosteal- bone and PL
249
Q

What capillary plexus has no loops in health?

A

dentogingival plexus

250
Q

What are the (6) reasons for stability of healthy gingiva?

A
  • shedding of epithelial cells- intact epithelial barrier- positive flow of gingival crevicular fluid- complement system- PMNs and macrophages- protective effects of antibodies
251
Q

What are the 4 histopathological stages in the development of gingivitis and periodontitis?

A
  • INITIAL LESION: subclinical stage of gingivitis- EARLY LESION: clinical early stage of gingivitis- ESTABLISHED LESION: chronic gingivitis- ADVANCED LESION: progression to periodontitis
252
Q

When does the initial lesion form? When the permeability increases, what leaks out of the vessels? What cells are present in the JE and what are in the CT?

A
  • occurs within 1-4 days of plaque development- carbon particles and serum proteins leak out of vessels- PMNs and monocytes in JE- lymphocytes in CT
253
Q

During the initial lesion, does the vascular density increase or decrease? The perivascular collagen? The gingival crevicular fluid volume?

A
  • vascular density increases- perivascular collagen decreases- gingival crevicular fluid volume increases
254
Q

True or false: The initial lesion stage is detectable clinically.

A

FALSE: It is not detectable clinically.

255
Q

Describe the vascular changes during the initial lesion.

A
  • dilation of vessels of the dentogingival plexus is induced by vasoactive mediators (histamine, IL-1, TNF)- gaps form between capillary endothelial cells, resulting in increased permeability- fluids and proteins move out of the capillary- gingival crevicular fluid flow rate increases
256
Q

In health, GCF is ___, but in disease, it is ___.

A
  • plasma transudate- inflammatory exudate
257
Q

The GCF constituents indicate ___ and ___. GCF flow rate ___ (increases/decreases) with clinical inflammation.

A
  • inflammatory changes- bacterial colonization- increases
258
Q

During the initial lesion, there is a cytokine-mediated up-regulation of ___ on endothelial cells. ___ adhere to the post-capillary venules and begin to migrate through the JE into the gingival sulcus. Chemotaxis is induced by ___ and ___.

A
  • adhesion molecules- PMNs- host factors (IL-8, C5a)- molecules released by bacteria (fMetLeuPhe)
259
Q

True or false: An initial lesion is an early response to plaque accumulation.

A

true

260
Q

Initial Lesion Summary:- ___ subjacent to JE- exudation of ___ into tissue and gingival sulcus- increased migration of ___ into the JE and gingival sulcus

A
  • vasculitis- fluid- leukocytes
261
Q

Initial Lesion Summary:- ___ present extravascularly- alteration of the ___ portion of JE- loss of ___

A
  • serum proteins- most coronal portion- perivascular collagen
262
Q

When does an early lesion occur? What cells are located subjacent to the JE and what cells are few in number? What cells undergo cytopathic alterations?

A
  • occurs within 4-7 days of plaque development- lymphocytes and PMNs subjacent to the JE- few plasma cells- fibroblasts
263
Q

True or false: Inflammation is clinically evident in an early lesion.

A

true

264
Q

In an early lesion, ___ destruction occurs which creates space for infiltrate. The ___ cells proliferate. ___ invade the coronal portion of the lesion.

A
  • collagen- basal cells of JE and SE- epithelial rete pegs
265
Q

During an early lesion, the ___ plexus remains dilated. There is a ___ (small/large) number of venules. The plexus ___ (is/is not) permeable.

A
  • dentogingival plexus- large number- is (extremely)
266
Q

In an early lesion, as the ___ invades the ___, the previously inactive capillary bed opens up and proliferates into the ___.

A
  • JE- CT- CT papillae
267
Q

Early Lesion Summary:- accentuation of the features of ___- accumulation of ___ immediately subjacent to JE- cytopathic alteration in resident ___

A
  • the initial lesion- lymphoid cells- fibroblasts
268
Q

Early Lesion Summary:- further loss of ___- early proliferation of ___- inflammatory changes ___ (are/are not) clinically evident

A
  • collagen network- basal cells of JE- are
269
Q

In an established lesion, increased swelling ___ (is/is not) clinically evident. There is ___ (increased/decreased) fluid exudation and leukocyte migration. ___ cells increase around blood vessels and in coronal CT. ___ loss continues as infiltrate expands.

A
  • is- increased- plasma cells- collagen
270
Q

In an established lesion, in addition to macrophages and serum proteins, what other cells are present?

A

T and B cells and plasma cells

271
Q

In an established lesion, what do activated T cells produce? Plasma cells? Fibroblasts?

A
  • T cells: cytokines and chemotactic substances- plasma cells: Ig and cytokines- fibroblasts: MMPs and TIMPs
272
Q

During an established lesion, what important conversion takes place? Describe this change.

A
  • conversion of JE to PE (permeable pocket epithelium)- JE and sulcular epithelium proliferate and migrate deeper into the CT; the sulcus deepens and the coronal portion of the JE is converted into PE
273
Q

True or false: PE is attached to the tooth surface.

A

FALSE: PE is not attached to the tooth surface.

274
Q

True or false: PE is loaded with PMNs.

A

true

275
Q

Established Lesion Summary:- persistence of features of ___- increased proportion of ___- presence of ___ in CT, JE, and gingival sulcus- continuing loss of ___

A
  • acute inflammation- plasma cells- extravascular immunoglobulins- collagen and matrix
276
Q

Established Lesion Summary:- proliferation and lateral extension of ___- early ___ formation may be evident- no apical migration of ___ and no ___ at this stage

A
  • JE- pocket- JE and no bone loss
277
Q

When does an advanced lesion occur?

A

beginning and duration are not known

278
Q

How is an advanced lesion different from an established lesion? (AKA what is the evidence of periodontitis?)

A
  • switch from T- to B-cell predominance signals conversion from gingivitis to periodontitis- destruction of CT attachment to root surface and apical migration of epithelial attachment indicates first clinical sign of periodontitis
279
Q

In an advanced lesion, where does bone destruction begin? How does it continue?

A
  • bone destruction begins around communicating blood vessels along crest of septum- apical proliferation of PE into the deep CT; the PE is not attached to the tooth
280
Q

Advanced Lesion Summary:- persistence of ___ features- increased proportion of ___ cells (approx. 50%)- extension of lesion into ___ with significant ___

A
  • established lesion features- plasma cells- alveolar bone and PL- bone loss
281
Q

Advanced Lesion Summary:- continued loss of ___ subjacent to PE- formation of ___ and apical migration of ___ from CEJ

A
  • collagen fibers and matrix- periodontal pocketing- JE
282
Q

What are the 3 common modifying factors of periodontitis?

A
  • diabetes- pregnancy/puberty/menopause- smoking
283
Q

What 5 things can modifying factors of periodontitis influence?

A
  • susceptibility to gingivitis and periodontitis- plaque growth and composition- clinical presentation- disease progression- response to periodontal therapy
284
Q

What are the 4 oral and periodontal effects of diabetes mellitus?

A
  • xerostomia- candida infections- periodontitis- multiple periodontal abscesses
285
Q

Is the incidence and severity of periodontitis greater in well-controlled or poorly-controlled diabetes?

A

poorly-controlled

286
Q

True or false: Periodontitis decreases insulin resistance.

A

FALSE: Periodontitis increases insulin resistance (glycemic control improved after periodontal therapy; diabetics with severe periodontitis have proteinuria and cardiovascular problems).

287
Q

What are the effects of diabetes on bacteria?

A
  • Spirochetes increase in poorly-controlled diabetes- P. intermedia, C. rectus, P. gingivalis in Type II diabetes- Capnocytophaga predominance in Type I diabetes
288
Q

What are the effects of diabetes on host response?

A
  • PMN FUNCTION AND CHEMOTAXIS IMPAIRED: PMN enzymes beta glucornidase and elastase increase in poor control; collagenase increases- CYTOKINES, MONOCYTES, AND MACROPHAGES: increase in PGE, IL-1beta, and TNF-alpha; advanced glycation end products create destructive phenotype of macrophages- CONNECTIVE TISSUE: decrease matrix synthesis by fibroblasts and osteoblasts; reactive oxygen species cause cell damage; AGE creates thickening of vascular endothelium, synthesis of wound healing steroids
289
Q

True or false: The effect of periodontal treatment on stable diabetics is the same as non-diabetics.

A

true

290
Q

What are the (5) effects of estrogen in pregnancy, puberty, and menopause?

A
  • affects salivary peroxidases- increases collagen metabolism and angiogenesis- increases vascular response and inflammatory mediators- increased gingiva inflammation- increased bleeding during menstrual cycle in women with gingivitis
291
Q

When is gingival inflammation the highest during pregnancy? What is pregnancy’s effect on the microbiota?

A
  • during 2nd and 3rd trimesters- increases P. intermedia; naphthoquinones from steroids used by Pi; increase in spirochetes
292
Q

What are the effects of pregnancy on the host that relate to periodontitis?

A
  • increase in vascular permeability, resulting in increased gingival exudate- decrease in keratinization- decrease in PMN chemotaxis and phagocytosis, antibodies, T-cell response
293
Q

When is periodontal treatment best during pregnancy? Should antibiotics be used?

A
  • during 2nd trimester- best to avoid use of antibiotics during pregnancy
294
Q

What syndrome does menopause lead to in 30% of women? What is this syndrome due to? How does this affect periodontal disease?

A
  • osteoporosis- due to decreased absorption and increased elimination of calcium- osteoporosis may not cause periodontal disease, but may affect severity of pre-existing disease
295
Q

What is the second risk factor for periodontitis?

A

tobacco smoking

296
Q

How does tobacco smoking effect the pockets? What other effects does it have on the periodontia?

A
  • deeper pockets and larger number of pockets- more attachment loss, including recession- more alveolar bone loss- more tooth loss- less gingivitis and bleeding on probing- more teeth with furcation involvement
297
Q

True or false: Tobacco smoking leads to less gingivitis and bleeding on probing.

A

true!

298
Q

What is the effect of tobacco smoking on bacteria?

A
  • smokers have more plaque- increase in AA, Tannerella forsythia, P. micros, P. gingivalis, C. rectus, and P. intermedia
299
Q

What is the effect of tobacco smoking on the host that relates to periodontitis?

A
  • lower BOP (decreased inflammation, decrease in blood vessels, increase in keratinization)- lower amounts of GCF in gingivitis- decreased PMN functions (migration, phagocytosis, ICAM)
300
Q

How does smoking affect the response to treatment?

A
  • smoking is associated with poorer reduction in probe depths and poorer attachment gain (without surgery)- smoking is associated with poorer response to periodontal surgical treatment- limited studies show that quitting smoking may lead to more favorable treatment outcome
301
Q

What is the definition of susceptibility?

A

the state of being easily affected, influenced, or harmed by something

302
Q

True or false: Different forms of periodontitis may have different etiologic factors.

A

true

303
Q

The magnitude and quality of the periodontal tissue changes are determined not only by the bacteria, but also by ___ and ___.

A
  • the patient’s genetics- environmental modifiers
304
Q

What 3 factors determine the clinical disease severity of periodontitis?

A
  • genetic modifiers- specific bacteria- environmental modifiers
305
Q

True or false: Periodontopathic bacterial flora is necessary but not sufficient for disease.

A

true

306
Q

What is the odds ratio that smoking will increase periodontitis? For diabetes?

A
  • smoking: 2.5-3.7- diabetes 2.8-3.4
307
Q

What is the definition of Mendalian inheritance? What are the modes of inheritance? What is it also known as?

A
  • the manner by which genes and traits are passed from parents to their children- autosomal dominant, autosomal recessive, x-linked dominant, and x-linked recessive- AKA classical or simple genetics or single gene disorders
308
Q

What is the definition of chromosome disorder?

A

an abnormal condition due to something unusual in an individual’s chromosomes

309
Q

What is the definition of complex gene disorders? What are some examples?

A
  • conditions caused by the effects of multiple genes in combination with lifestyle and environmental factors- ex. cardiovascular disease, diabetes mellitus, and destructive periodontal disease
310
Q

What is the definition of polymorphism?

A

exists when two or more different phenotypes exist within different individuals within the same population; in the context of genetics, it refers to a region of the genome that varies between individual members of the population in such proportions that the rarest of them cannot be maintained just by recurrent mutation

311
Q

What is the definition of SNP? How often are they seen?

A
  • single nucleotide polymorphisms are the most common type of genetic variation; each represents a difference in a single nucleotide- occur normally throughout a person’s DNA, once in every 300 nucleotides so there are roughly 10 million SNPs in the human genome
312
Q

What 3 things do complex genetic disorders involve?

A
  • multifactorial (polygenic) interactions- gene-gene interactions- gene-environment interactions
313
Q

What are the 5 characteristics of complex gene traits?

A
  • common in population- no clear familial transmission- adult age onset- environmental factors etiologic too- combination of multiple small genetic and environmental factors
314
Q

Which type (simple or complex) genetic disease is described?- single etiologic gene- gene has major effect- simple pattern of transmission

A

simple genetic disease

315
Q

Which type (simple or complex) genetic disease is described?- phenotype usually less modified by environmental interactions

A

simple genetic disease

316
Q

Which type (simple or complex) genetic disease is described?- chronic onset

A

complex genetic disease

317
Q

Which type (simple or complex) genetic disease is described?- many genes may contribute to etiology- contribution of each gene is individually small and cannot cause disease alone- complex pattern of transmission

A

complex genetic disease

318
Q

Which type (simple or complex) genetic disease is described?- usually acute onset

A

simple genetic disease

319
Q

Which type (simple or complex) genetic disease is described?- phenotype continuum; environmental factors can be very important to phenotype

A

complex genetic disease

320
Q

What 3 types of defects may make a person more susceptible to periodontitis?

A
  • structural defects (mucosa, collagen)- immune response defects (cytokines)- white blood cell defects (neutrophils, macrophages)
321
Q

What are the 4 reasons why it is not realistic to expect a single gene polymorphism (SNP) will be diagnostic for a complex genetic disease?

A
  • no single gene contributes enough to cause disease alone (in contrast to Mendelian disease)- environmental factors are important and required to cause disease- need to study many (thousands) of people in standardized way to identify an association between a SNP and disease state- human populations are mixed in terms of gene polymorphisms and environmental exposures, making studies difficult to control
322
Q

Successful management of periodontal disease depends on the ability of a clinician to do what 3 things?

A
  • accurate diagnosis of periodontal disease- predict the effect of the systemic status of the patient on the course of the disease- confirm the prediction with assessment of therapeutic outcomes
323
Q

What is the definition of periodontal diseases?

A

a diverse family of complex and distinct pathological entities found within the periodontium that are the result of a variety of etiologies; encompasses both gingival diseases and destructive periodontal diseases

324
Q

What are the 6 characteristics common to all gingival diseases?

A
  • signs and symptoms that are confined to the gingiva- the presence of dental plaque to initiate and/or exacerbate the severity of the lesion- clinical signs of inflammation- clinical signs and symptoms associated with stable attachment levels on a periodontium with no loss of attachment- reversibility of the disease by removing the etiology(ies)- possible role as a precursor to attachment loss around teeth
325
Q

True or false: Not all periodontitis becomes gingivitis, but most gingivitis started as periodontitis.

A

FALSE: Not all gingivitis becomes periodontitis, but most periodontitis started as gingivitis.

326
Q

What are the 4 systemic factors that can modify gingival disease?

A
  • the endocrine system (endocrinotropic)- blood dyscrasias- medications- nutrition
327
Q

What are the 5 endocrinotropic gingival diseases?

A
  • puberty-associated gingivitis- menstrual cycle-associated gingivitis- pregnancy-associated gingivitis- pregnancy-associated pyogenic granuloma- diabetes mellitus-associated gingivitis
328
Q

What gingival disease is associated with blood dyscrasias? Describe it.

A
  • leukemia-associated gingivitis- gingival lesions are primarily found in acute leukemia; reductions in dental plaque can limit the severity of the lesion
329
Q

What gingival disease is modified by nutrition? Describe it.

A
  • ascorbic acid-deficiency gingivitis- malnourished individuals have a compromised host defense system which may make individuals susceptible to infectious diseases; human studies have failed to show a relationship between nutrition and periodontal diseases
330
Q

What are the 4 types of destructive periodontal diseases?

A
  • chronic periodontitis- aggressive periodontitis- periodontitis as a manifestation of systemic diseases- necrotizing periodontal diseases
331
Q

What are the (5) clinical manifestations of chronic periodontitis?

A
  • pocket formation- loss of attachment- bleeding/suppuration- bone loss- tooth mobility and drifting
332
Q

What age group is chronic periodontitis most common in? What type of calculus is associated with chronic periodontitis?

A
  • adults (although it can occur in children and adolescents)- subgingival calculus
333
Q

What is the speed of progression of chronic periodontitis? What is it associated with or modified by?

A
  • slow to moderate progression- local predisposing factors (ex. tooth-related), systemic disease, or environmental factors
334
Q

What are the 2 ways to classify chronic periodontitis?

A
  • EXTENT: localized (if 30% mouth)- SEVERITY: slight (1-2 mm CAL), moderate (3-4 mm CAL), and severe (5+ mm CAL)
335
Q

How is aggressive periodontitis classified?

A

localized or generalized

336
Q

What are the (3) common features of aggressive periodontitis?

A
  • systemically healthy- rapid attachment loss and bone destruction- familial aggregation
337
Q

What are the (6) secondary features of aggressive periodontitis?

A
  • generally, but may not be universally, present- microbial deposits are inconsistent with the amount of periodontal destruction- elevated Actinobaccillus actinomycetemcomitans and Porphyromonas gingivalis- phagocyte abnormalities- hyper-responsive macrophage phenotype- progression may be self-arresting
338
Q

What age group is most affected by localized aggressive periodontitis? What type of serum antibody response is present toward infecting agents? Where is the disease localized?

A
  • usually around puberty- robust serum antibody response- localized first molar/incisor presentation (interproximal attachment loss on at least 2 permanent teeth, one of which is a molar; involving no more than 2 teeth other than first molars and incisors)
339
Q

What age group is most affected by generalized aggressive periodontitis? What type of serum antibody response is present toward infecting agents? Describe the location and progression of the disease.

A
  • usually affects persons under 30 but patients may be older- poor serum antibody response- generalized interproximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors- pronounced episodic nature of destruction of attachment and bone (happens every few years and then stops)
340
Q

What types of disorders is periodontitis associated with?

A
  • hematologic disorders- genetic disorders
341
Q

Describe the periodontium in a patient with Down syndrome.

A
  • severe inflammation- accelerated attachment loss- PMN chemotaxis and killing defects
342
Q

Describe the periodontium in a patient with Papillon-Lefevre syndrome.

A

rapid periodontal destruction around primary and permanent teeth which occurs before puberty

343
Q

Describe the periodontium in a patient with Chediak-Higachi syndrome.

A

rapid periodontal destruction around primary and permanent teeth which occurs before puberty

344
Q

Describe the periodontium in a patient with Ehlers-Danlos syndrome (Types IV and VIII).

A

aggressive periodontitis (primary and permanent dentition); fragility of gingiva, excessive hemorrhage

345
Q

What are the 2 types of necrotizing periodontal disease? What is the difference between the two?

A
  • NECROTIZING ULCERATIVE GINGIVITIS (NUG): limited to gingival tissues- NECROTIZING ULCERATIVE PERIODONTITIS (NUP): lesion confined to periodontal tissues
346
Q

Describe the early clinical signs of necrotizing periodontal disease.

A
  • necrotic lesion of the papilla initially, then progressing to gingival margin- punched-out appearance- spontaneous bleeding- pain
347
Q

Describe the signs of an advanced necrotizing periodontal disease lesion.

A
  • lack of deep pockets- merging of papillary and marginal involvement- characterisitc fetor (smell)- central necrosis results in crater formation- involvement of periodontal ligament and alveolar bone (NUG -> NUP)
348
Q

For necrotizing ulcerative periodontitis, involvement of palatal mucosa is called ___. There is involvement of regional ___. It is typically related to ___ and may develop into ___.

A
  • necrotizing stomatitis- regional lymph nodes- severely compromised immune system- life-threatening situation
349
Q

Describe the (3) symptoms of necrotizing ulcerative periodontitis.

A
  • fever and malaise- white membrane of desquamated cells, bacteria, and saliva proteins- membrane can be easily removed
350
Q

Differentiate between gingival, periodontal, and pericoronal abscesses.

A
  • GINGIVAL: localized, acute inflammation/vital pulp; marginal and interdental tissues- PERIODONTAL: localized, acute, or chronic inflammation, vital pulp; moderate/deep pockets and possible bone destruction- PERICORONAL: localized, acute inflammation, vital pulp; crown of partially erupted tooth
351
Q

What is the definition of epidemiology?

A

study of disease origin and spread and pattern of disease development

352
Q

What is the difference between prevalence and incidence?

A
  • PREVALENCE: the number of cases of a disease or condition per population at risk at a particular point in time- INCIDENCE: the number of new cases of a disease or condition over a specified period of time
353
Q

Is gingival inflammation more common in males or females?

A

males

354
Q

What is the CPITN? What is it used for?

A
  • Community Periodontal Index of Treatment Needs- can be used as part of a global surveillance system to compare periodontal health in differing countries; provides information concerning the type of disease and therefore the extent of therapy
355
Q

How does the coding work for CPITN?

A
  • the mouth is divided into sextants defined by tooth number- index teeth in each sextent are probed and pocket depth, subgingival calculus, and BOP is determined
356
Q

What are the index teeth for adults >20 years?

A

2, 3, 8, 14, 1531, 30, 24, 19, 18

357
Q

What do the codes 0, 1, 2, 3, and 4 in CPITN stand for?

A
  • 0: healthy- 1: bleeding observed after probing- 2: calculus detected during probing- 3: pocket 4-5 mm- 4: pocket 6 mm or more
358
Q

American males ages 35-44 recorded the largest number of CPITN code 4 in the world. What is this code?

A

pocket 6 mm or more

359
Q

Approximately what % of Americans are affected by advanced periodontal disease (>5 mm pocket)?

A

13%

360
Q

Which gender has more attachment loss?

A

male

361
Q

Is localized or generalized aggressive periodontitis more common?

A

localized

362
Q

What % of adults has moderate chronic periodontitis? What % of seniors (age 65+) has moderate chronic periodontitis?

A
  • 20%- 50%
363
Q

Is localized aggressive periodontitis more common in Caucasians or African Americans? What is the prevalence of generalized?

A
  • African Americans- 0.13%

AU14 - Perio Exam 1 (1 decks)

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