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Jane (and Margie)'s Veterinary Dentistry export questions > Carranza periodontology > Flashcards

Carranza periodontology Flashcards

1
Q

What is the turnover time for junctional epithelium?

A

4 to 6 days

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2
Q

Under normal circumstances, the gingival sulcus should be how deep?

A

0 mm (or close to it), but this is only possible in germ-free animals, lab settings

-the histologic depth of a sulcus does not need to be exactly equal to the depth of penetration of the periodontal probe

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3
Q

Attached gingiva: width?

A

distance between MGJ and projection on the external surface of the bottom of the sulcus, or periodontal pocket (different than width of keratinized gingiva), is different throughout the mouth
The width of attached gingiva increases with age (?)

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4
Q

What are the layers of stratified squamous epithelium?

A

Stratum corneum
Stratum granulosum

Stratum spinosum

Stratum basale

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5
Q

What is the difference between orthokeratinized, parakeratinized, and nonkeratinized epithelium?

A

Ortho- no nuclei in the stratum corneum and well-defined stratum granulosum (only some areas of gingiva are this)
Para- stratum corneum retains pyknotic nuclei, keratohyaline granules dispersed (not giving rise to a granulosum)

Non- has neither corneum or granulosum, superficial cells have viable nuclei

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6
Q

What does gingival epithelium consist of (cells)?

And what is the principle cell type of this tissue?

A

Overlying stratified squamous epithelium, underlying central core of connective tissue (primarly composed of collagen fibers and ground substance)

KERATINOCYTE

(also has nonkeratinocytes, including langerhans cells, merkel cells, and melanocytes)

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7
Q

How are keratinocytes interconnected?

A 
By desmosomes (structures on the cell periphery)- tonofilaments
Less frequently, they can have tight junctions, in which the membranes of the adjoining cells are fused (ions and small molecules can pass between cells)
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8
Q

Melanocytes are what kind of cells?

And are located in what layers of the gingival epithelium?

A
  • Dendritic cells

- basal and spinous layers

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9
Q

What enzyme is closely related to the degree of keratinization? (contained in the upper layer of the stratum spinosum)

A

Lysosomes

Keratinization begins in the stratum spinosum!

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10
Q

What are Langerhans cells and where are they located?

A

Located among keratinocytes at suprabasal levels

Are modified monocytes (macrophages with possible antigenic properties), antigen presenting cells for lymphocytes

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11
Q

What are Merkel cells?

A

located in deeper layers of epithelium
harbor nerve endings, connected to adjacent cells by desmosomes

TACTILE PERCEPTORS

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12
Q

How is the epithelium joined to the underlying connective tissue?

A

Basal lamina

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13
Q

Oral epithelium (outer) is how keratinized? (which is the most, and which is the least?)

A

Para or keratinized, majority is para
-palate, gingiva, ventral aspect of tongue, cheek (from most to least)

-degree of keratinization diminishes with age and onset of menopause

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14
Q

Sulcular epithelium!
-What type?

  • what cell is missing in this?
  • acts as?
A

Thin, non-keratinized stratified squamous (lacking granulosum and corneum), but keratinizes if exposed to the oral environment
-No Merckel cells normally

-semipermeable membrane through which injurious bacterial products can pass into the gingival and tissue fluid

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15
Q

Junctional epithelium
1-consists of?

2- is how thick?

3-is thickest at what point?

4- where is the apical termination in healthy tissue?

A

1-stratified squamous nonkeratinizing epithelium
2- 3-4 layers in early life, but layers increase with age

3- tapers from its coronal end, so only a couple cells wide at its apical termination

4- Apical termination is at the cementoenamel junction in healthy tissue

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16
Q

Junctional epithelium is formed by the confluence of what?

A

The REE and oral epithelium (but REE is not essential for its formation)

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17
Q

What cells are consistently present in junctional epithelium?

A

PMNs!, with a substantial increase seen with accumulation of dental plaque and gingival inflammation

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18
Q

How is the junctional epithelium attached to the tooth surface?

A

By means of an internal basal lamina, which consists of a lamina densa (next to enamel), and lamina lucida (to which hemidesmosomes are attached)
Organic strands from enamel appear to extend into lamina densa

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19
Q

Who is the father of dentistry?

A

Pierre Fauchard

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20
Q

Attachment of junctional epithelium to the toth is reinforced by?

A

Gingival fibers, for this reason, junctional epi and gingival fibers are considered as a functional unit, called the dentogingival unit

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21
Q

So, how does junctional epithelium contribute to defense?

A

epithelial barrier
allows access of gingival fluid, inflammatory cells, and components of host defense to the gingival margin

Exhibit rapid turnover!

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22
Q

Development of the gingival sulcus: proceeds how?

A

after enamel formation is complete, it is covered with the REE, and when tooth penetrates the oral environment, the REE unites with the oral epithelium and transforms into the junctional epithelium
-as tooth erupts, this united epithelium condenses along the crown, and the ameloblasts (inner layer of REE) gradually become squamous epi cells

-transformation of REE into Junctional eli occurs in an apical direction

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23
Q

How do keratinization and gingivitis affect mitotic rate?

A

Higher mitotic rate in nonkeratinized areas

Also higher rate with gingivitis

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24
Q

What layers does new cell formation occur in?

A

Spinosum and basale

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25
Q

How do epi cells participate in immunity?

A

Increased proliferation
alteration of cell-signaling events

changes in differentiation and cell death

alteration of tissue homeostasis

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26
Q

What is a cuticle?

And what are three coatings of developmental origin in the tooth?

A

1- thin, acellular structure with a homogenous matrix

2- REE, coronal cementum, dental cuticle

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27
Q

What is the main route of diffusion for gingival fluid?

A

Thru the basement membrane, thru the relatively wide intracellular spaces of the junctional epithelium, and then into the sulcus

-Is a transudate to exudate (exudate in inflammation)

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28
Q

Gingival connective tissue!
1- Major components?

2-CT of gingiva is known as?

3- Contains what two layers?

A

1- collegen fibers, fibroblasts, vessels, nerves and matrix

2- Lamina Propria

3- papillary layer (subjacent to epithelium, papillary projections)

Reticular layer, contiguous with periosteum

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29
Q

What type of collagen forms the bulk of lamina propria?

A

Type 1

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30
Q

Gingival fibers: arranged in what three groups?

A

1- Gingivodental group: on facial, lingual and interproximal surfaces, embedded in cementum just beneath the epi at the base of the sulcus
2- Circular group: encircle the tooth in a ringlike fashion, course through the connective tissue of the marginal and interdental gingiva

3- Transseptal group: located interproximally, extend between cementum of approximating teeth

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31
Q

Connective tissue of marginal gingiva! Contains collagen fiber bundles (type 1!) called gingival fibers! Functions are???

A

1- brace marginal gingiva firmly against tooth
2- provide the rigidity necessary to withstand mastication forces

3- unite the free marginal gingiva with the cementum of the root and the adjacent attached gingiva

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32
Q

What is the preponderant cellular element in gingival connective tissue?
What do they do?

A

Fibroblast
-they synthesize collagen and elastic fibers, as well as the glycoproteins and glycosaminoglycans of the amorphous intercellular substance

-also regulate collagen degradation through phagocytosis and secretion of collagenases

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33
Q

What cells are numerous in the CT of oral mucosa and gingiva?

A

Mast cells!

Also has fixed macrophages, histiocytes, adipose cells, and eosinophils (rare)

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34
Q

Does gingival epithelium (epithelial cells) play a role in immunity?

A

Yes, active role in innate host defense

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35
Q

Junctional Epithelium

A
  • Adheres to enamel; collar-like band of stratified squamous (non-keratinized)
  • Forms base of sulcus; separates PDL from oral environment
  • widest at bottom of sulcus (15-20 cells); narrows apically
  • Part of host defense to plaque or bacteria insult; fluid constantly flowing as part of defense (exudate)
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36
Q

Three reasons junctional epithelium prevent pathogenic bacterial flora

A

1- Firmly attached to tooth surface, so epi barrier
2- allows access of gingival fluid, inflammatory cells, and host defenses

3- rapid turnover

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37
Q

after enamel formation is complete, the enamel is covered by the REE (reduced enamel epithelium), which is attached to tooth by basal lamina and hemidesmosomes. When the tooth penetrates the oral mucosa, the REE unites with the oral epi and forms the junctional epithelium

A

continually self-renewing structure with mitotic activity occurring in all cell layers

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38
Q

Gingival fluid (sulcular fluid)

A

transudate or exudate
in health, amount is very small, increases with disease/inflammation

Main route of diffusion: through the basement membrane, through the wide intracellular spaces of the junctional epithelium, and then into the sulcus

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39
Q

Gingival connective tissues

A 
Main components:
collagen fibers (60%), fibroblasts (5%), vessels, nerves, and matrix (35%)

Fibroblast is main cellular element, mesenchymal origin

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40
Q

Connective tissue of the gingiva is known as the lamina propria: consists of what two layers?

A

1- Papillary layer: subjacent to epithelium, consists of papilllary projections b/w rete pegs
2- Reticular layer- contiguous with periosteum of alveolar bone]=

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41
Q

Gingival fibers: arranged in what three groups?

A

1- Gingivodental group: facial, lingual and interproximal surfaces, embedded in cementum just beneath the epi at the base of the sulcus
2- Circular group: encircle the tooth in a ringlike fashion, marginal and interdental gingiva

3- Transseptal group: located interproximally, extend between cementum of approximating teeth

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42
Q

Three sources of blood supply to the gingiva

A

1- Supraperiosteal arterioles
2- Vessels of the PDL

3- Arterioles which emerge from the crest of the interdental septa

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43
Q

Active eruption vs passive eruption

A

Active- movement of the teeth in the direction of the occlusal plane (apposition of bone accompanies this stage)
Passive= exposure of the teeth by apical migration of the gingiva

(anatomic crown/root vs clinical crown root)

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44
Q

RANKL vs OPG

A 
RANKL= activates osteoclasts
OPG= antagonizes RANKL binding
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45
Q

Definition of periodontitis

A

“an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms, resulting in progressive destruction of the PDL and alveolar bone with increased probing depth formation, recession, or both.”

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46
Q

Chronic periodontitis

A

Localized: less than 30% of sites
Generalized: >30% of sites

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47
Q

Endodontic-Periodontal lesions

A

Pulpal necrosis precedes periodontal changes. A periapical lesion may drain into the oral cavity thru the PDL and resulting in destruction of the PDL and alveolar bone

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48
Q

Periodontal-Endodontic lesions

A

Bacterial infection from a periodontal pocket may spread thru accessory canals to the pulp; infection may reach the pulp thru the apical foramen too!

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49
Q

Combined endo-perio lesions

A

when pulpal necrosis and a periapical lesion appear on a tooth that is also periodontally involved

ENDO SHOULD ALWAYS BE CONTROLLED FIRST!

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50
Q

Most reliable study design?

Most common study design?

A
  1. Randomized controlled trials

2. Case-control and cohort studies

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51
Q

Measuring the occurrence of diseases

1- Prevalence?

A

1- Number of individuals that have a particular condition within a defined population

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52
Q

Risk?

A

probability that an individual or a site will develop a particular condition or disease during follow-up
When risk is reported, it should be accompanied by a specific time period

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53
Q

Odds

A

is the probability that an event happened divided by the probability that an event did not happen
This is often easier to estimate that probabilities, so often reported in studies

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54
Q

Incidence rates

A

This reflects the number of disease occurrences per time unit per person
They apply an element of time (The denomenator is time)

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55
Q

Gingival crevicular fluid

Can normally change with circadian rhythms, sex hormones, smoking, mechanical stimulation

A

1- cellular elements include bacteria, desquamated epi cells, and leukocytes (PMNs, lymphocytes, monocytes)
2- Higher glucose in GCF than in serum (4X)

3- TP much lower in GCF, doesn’t change with inflammation

4- Total amount of GCF is greater with inflammation

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56
Q

First stages/manifestations of gingivitis

A

vascular changes, dilated capillaries and increased blood flow, not clinically apparent (subclinical) Leukocytes (PMNs) leave capillaries (migrate, diapedesis)

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57
Q

What is Stage II gingivitis?

A

Stage II gingivitis or early lesion occurs approx. 1 week after plaque accumulation. It is marked clinically by erythema, BOP due to increased proliferation of capillaries and capillary loops btw rete ridges. Predominant leukocytes now become lymphocytes (T cells). Increased collagen destruction of circular and dentogingival fiber grps.

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58
Q

What is stage III gingivitis?

A

Established lesion gingivitis is marked by impaired venous return due to engorged and congested blood vessels which leads to anoxemia. Characterized by the presence of plasma cells and B lymphocytes and IgG. This occurs typically 2-3 weeks after plaque accumulation.

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59
Q

Stage IV gingivitis

A

Fibrosis of gingiva and widespread manifestations of inflammatory and immunopathologic tissue damage. Plasma cells dominate connective tissue and neutrophils dominate the junctional epi

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60
Q

Localized marginal gingivitis

A

confined to one or more areas of marginal gingiva

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61
Q

Localized diffuse gingivitis

A

extends from margin to the mucobuccal fold in a limited area

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62
Q

Localized papillary gingivitis

A

confined to one or more interdental spaces in a limited area

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63
Q

Generalized marginal gingivitis

A

involves gingival margins in relation to all the teeth, interdental papilla usually affected

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64
Q

generalized diffuse gingivitis

A

involves entire gingiva

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65
Q

Histologic evaluations on animals showed what in the early stages of gingivitis?

A

expression of cytokines responsible for connective tissue breakdown (MMPs) is ubiquitous

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66
Q

Actual vs apparent position of gingiva

A

Actual= level of the coronal end of the epithelial attachment on the tooth

Apparent= level of the crest of the gingival margin

Severity of recession measured by actual position!

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67
Q

Drugs responsible for drug induced gingival enlargement?

A

Calcium channel blockers, anticonvulsants, immunosuppressants

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68
Q

Pericoronitis

A
  • Inflammation of a gingival flap (operculum – little flap of skin that goes over tooth) over the crown/occlusal surface of an erupting tooth (i.e. third molar)
  • Debris/food trapped ® inflammation ® +/- infection
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69
Q

Pemphigoid

A

applies to a number of cutaneous, immune-mediated, subepithelial bullous diseases characterized by a separation of the basement membrane zone

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70
Q

Healthy gingiva microorganisms?

Disease gingiva?

A 
Healthy= coccoid cells and straight rods
Diseased= increased numbers of spirochetes and motile rods
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71
Q

Formation of periodontal pocket

A

host’s immunoinflammatoryresponse unleashes mechanisms that lead to collagen and bone destruction; related to various cytokines

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72
Q

Two mechanisms associated with collagen loss

A

1- collagenases and other enzymes become extracellular and destroy collagen (these enzymes are called MMPs)
2- Fibroblasts phagocytized collagen fibers

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73
Q

Extension of the juctional epithelium along the root requires?

A

The presence of healthy epithelial cells, so marked degeneration of junctional epi impairs rather than accelerates pocket formation

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74
Q

Soft tissue wall of a periodontal pocket

A

C.T. edematous and densely infiltrated with plasma cells, lymphocytes, and PMNs. B.V.’s increased in number and are dilated and engorged. Necrotic foci are seen. Junctional epi at base of pocket in much shorter than a normal sulcus. Most severe degeneration is along the lateral wall of the pocket

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75
Q

Are sharpey’s fibers affecting in a periodontal pocket?

A

Yes, undergo degradation. Bacteria then penetrate root, and can been seen up to the CDJ
Cementum is very thin in cervical regions, so scaling and root planing may remove it completely, exposing dentin

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76
Q

Dominant microorganism in root surface caries?

A

Actinomyces viscosus

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77
Q

Transeptal fibers in suprabony vs infrabony pockets?

A 
Suprabony= arranged horizontally in the space b/w the base of the pocket and alveolar bone
Infrabony= oblique rather than horizontal, extend from cementum beneath base of pocket along the alveolar bone and over crest to the cementum of adjacent tooth
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78
Q

Bone destruction in periodontal disease

A

Not a process of bone necrosis, involves the activity of living cells along viable bone. Osteoclasts. (# of osteoclasts does not correlate with amount of inflammation, but does correlate with distance from the apical border of the inflammatory infiltrate to the alveolar bone crest)

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79
Q

Buttressing bone formation

A

areas of bone formation found immediately adjacent to sites of active bone resorption and along trabecular surfaces at a distance from the inflammation

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80
Q

How does the periodontium respond to an increase in the magnitude of occlusal forces?

A

With a widening of the pdl space, an increase in the # and width of PDL fibers, and an increase in density of the alveolar bone

Constant pressure on bone is more injurious than intermittent force

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81
Q

Traumatic occlusion defined by?

A

whether it produces periodontal injury! (not how the teeth occlude)

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82
Q

slightly excessive pressure?

VS. slightly excessive tension?

A

1- stimulates resorption of alveolar bone, widening of PDL space (severe pressure causes undermining resorption, necrosis of PDL and bone)
2- causes elongation of the PDL and apposition of alveolar bone, enlarged blood vessels (severe tension causes resorption of bone and widening of PDL)

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83
Q

Areas of periodontium most susceptible to injury from excessive occlusal forces?

A

Furcations

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84
Q

Red complex in people?

A

P. Gingivalis, tannerella forsythia, and treponema denticola

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85
Q

attachment loss and bone loss are associated with what bacteria?

A

Increase in gram negative, anaerobic

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86
Q

Specific plaque hypothesis for chronic periodontal disease?

A

implies that although a general increase occurs in the proportion of gram-neg microorganisms in teh subgingival plaque, it is the presence of increased proportions of the “red complex” that precipitates attachment and bone loss

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87
Q

dentogingival junction

A
  • anatomical and functional interface between the gingiva and the tooth structure
  • 3 epithelial types within:

1) gingival
2) sulcular
3) junctional
- forms from the epithelial cuff
- under healthy cnditions it is bounded laterally by the oral sulcular epithelium and the enamel of the tooth.
- its coronal border is the free gingival margin and its apical aspect is the coronal aspect of hte junctional epithelium.
- AKA bounded by the histological sulcus in absolute health

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88
Q

Junctional epi as a function of attaching to the tooth

A

Unique epi structure b/c surface cells are specialized to attach to the tooth, so unlike other epi cells in body, it cannot slough. Cells at basal layer continually divide and move to within two or three cell layers of the tooth surface and then migrate coronally, parallel to the tooth surface to eventually reach the floor of the sulcus to be sloughed off in the gingival crevice

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89
Q

extracellular spaces of junctional epi compared to other epi?

A

Extracellular spaces b/w the junctional epi are greater than other tissues, with intercellular spaces comprising about 18% of the volume.
Making junctional epi LEAKY

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90
Q

Early lesion of periodontitis?

A

-after 1 wk of plaque build-up -vasodilation, increased GCF flow, transmigrating neutrophils increase -predominant cells are neutrophils and lymphocytes (T-cells) -collagen fibers begin to be destroyed in areas apical and lateral to the junctional epi -edema of gingival tissues

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91
Q

Established lesion of periodontitis

A

chronic gingivitis -significant inflammatory cell infiltrate -collagen depletion continues -neutrophils accumulate and are a major releaser of MMPs -Junctional and sulcular epi form a pocket epithelium that is not firmly attached to the tooth, has large #s of neutrophils, and is permeable -Still reversible!

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92
Q

Advanced lesion of periodontitis

A

-marks transition from gingivitis to perio -neutrophils dominate in pocket epi, and plasma cells dominate in connective tissues -Junctional epi migrates apically to the collagen depleted areas below it -Osteoclastic bone resorption starts, bone retreats from advancing inflammatory front to prevent spread of bacteria into bone

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93
Q

Lipopolysaccarides

A

found on outer membrane of gram-neg bacteria -act as endotoxins -elicit strong immune responses -immune system reacts with toll-like receptors (TLRs) which recognize MAMPs (microbe-associated molecular patterns) -particular key importance in initiating and sustaining inflammatory responses

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94
Q

Bacterial enzymes and noxious products

A

Noxious agents: ammonia, hydrogen sulfide, butyric and propionic acid -these have a profound affect on host cells Bacteria also produce proteases, which breakdown structural proteins of the periodontium -gigipains

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95
Q

Key mediators that orchestrate host responses are?

A

Cytokines MMPs Prostanoids

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96
Q

Cytokines

A
  • soluble proteins and act as messengers to transmit signals from one cell to another - bind to receptors on target cells and initiate intracellular signaling cascades -can work in a positive feedback cycle -produced by a large number of cells (lymphocytes, neutro, macro, fibroblasts, epi cells, …) -mediate connective tissue and alveolar bone destruction thru induction of fibroblasts and osteoclasts to produce proteolytic enzymes (MMPs)
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97
Q

Prostaglandins

A

-group of lipid compounds derived from arachidonic acid -arachidonic acid metabolized by COX-1 and 2 to generate the prostanoids PGs are mediators of inflammation -PGE2 results in vasodilation and induces cytokine production COX2 is upregulated by cytokines and LPS PGE2 results in induction of MMPs and osteoclastic bone resorption

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98
Q

MMPs (matrix metalloproteinases)

A

-proteolytic enzymes that degrade extracellular matrix such as collagen, gelatin, and elastin -produces by many cells -secreted in a latent form (inactive) and activated by proteolytic cleavage, which is achieved with proteases (like cathepsin G, made by neutophils) -inhibited by the tetracycline class of Ab’s

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99
Q

Cells primarily responsible for PGE2 production are?

A

Macrophages and fibroblasts

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100
Q

How does the epithelium play an active role in innate immunity?

A

-by expressing antimicrobial peptides, called defensins -secrete chemokines to attract neutrophils

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101
Q

Bone resorbs so that there is always a width of ? of noninfiltrated connective tissue overlying the bone?

A

0.5 to 1 mm

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102
Q

Key system for controlling bone turnover?

A

rank/rankl/opg

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103
Q

RANK

A

-cell surface receptor expressed by osteoclast progenitor cells as well as mature osteoclasts

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104
Q

RANKL

A

ligand that binds to RANK and is expressed by bone marrow stromal cells, osteoblasts, and fibroblasts

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105
Q

Bonding of RANKL to RANK results in?

A

osteoclast differentiation and activation and thus bone resorption

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106
Q

OPG?

A

another ligand that binds to RANK
-produced by bone marrow stromal cells, osteoblasts, and PDL fibroblasts.

-inhibits differentiation of osteoclasts

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107
Q

What regulates the expression of RANKL and OPG?

A

IL-1beta
TNF-alpha

  • T cells express RANKL
  • In periodontitis, there is increased levels of IL-1b and TNF-a and increasing numbers of T-cells
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108
Q

What mediates the resolution of inflammtion?

A

Lipoxins, resolvins, protectins (proresolving lipid mediators)

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109
Q

Lipoxins

A

lipoxygenase-derived eicosanoids and are generate from arachidonic acid
-inhibit neutrophil recruitment, chemotaxis, and adhesion

-signal macrophages to phagocytose the remnants of apopotic cells without generating an inflammatory response

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110
Q

Resolvins and protectins

A

Resolvins- derived from omega-2 FA’s (EPA, DHA), inhibit neutrophil infiltration and migration, inhibit production of proinflammatory mediators, and have antiinflammatory effects

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111
Q

Innate immunity

A

saliva, GCF, epithelial keratinocytes, commensal microflora

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112
Q

Clinical ebb and flow of periodontitis is a reflection of fluctuations in?

A

Adaptive immunity

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113
Q

Pathogen recognition and activation of cellular innate responses

A

Macrophages and dendritic cells express a range of PRRs (pattern recognition receptors) that interact with MAMPs (microbe associated molecular patterns) to signal immune responses
EX: TLRs with bacterial LPS

Some non-immune cells also express PRRs, like epi cells and fibroblasts

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114
Q

Adaptive immunity

A

Slower than innate, relies on interactions b/w antigen-presenting cells and T and B lymphocytes

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115
Q

Population of leukocytes in periodontium of gingivitis and stable periodontal lesions is?
Population in active periodontitis?

A

T cells, clustered around blood vessels

2- B-cells and plasma cells, associated with pocket formation and progression of disease

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116
Q

Antigen presenting cells of the periodontium?

A

B-cells, macrophages, and two types of dendritic cells (dermal dendritic cells, langerhans cells)
They express MHC Class II molecules

Expression of MHC can be induced in other cells as well

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117
Q

Significance of antibodies in periodontitis?

A

Unclear, not sure if they have a protective function or if they participate in disease pathogenesis

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118
Q

Calculus?

A

Mineralized dental plaque, hardened by precipitation of mineral salts from saliva (supragingival) and CGF (subgingival)
-generally starts extracellulary, but can start intracellulary

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119
Q

Materia alba

A

white or cream-colored cheesy mass that can collect over dental biofilm on unclean, neglected teeth; it is composed of food debris, mucin, and bacteria.

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120
Q

Biofilms

A

composed of microbial cells encased within a matrix of extracellular polymeric substances (EPS) such as polysaccharides, proteins, and nucleic acids
Plaque is a biofilm

Intercellular matrix consists of organic and inorganic materials derived from saliva, GCF, and bacterial products

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121
Q

Organic constituents of the biofilm matrix?

A

polysaccharides, proteins, glycoproteins, lipid material, and perhaps DNA

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122
Q

What are the primary inorganic components of plaque?

A

Calcium and phosphorous (traces of sodium, potassium and flouride)

Dental plaque is composed primarily of microorganisms!

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123
Q

Phases of the process of plaque formation

A

1- formation of pellicle on tooth surface (bacteria adhere to acquired enamel pellicle)
2- initial adhesion/attachment of bacteria (interaction between microbial cell surface adhesin molecules and receptors in the salivary pellicle)

3- colonization and plaque maturation

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124
Q

Old vs new plaque, bacterial growth rate

A

Growth much slower in older plaque, because nutrients become limiting for much of the plaque biomass

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125
Q

Viruses replicate only in?

A

When they are present within eukaryotic or prokaryotic cells (not on their own)

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126
Q

Non-specific plaque hypothesis

A

maintains that periodontal disease results from the “elaboration of noxious products by the entire plaque flora”
- but this relies on quantities of plaque causing disease, which does not appear to be the case

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127
Q

Ecologic plaque hypothesis

A

both the total amount of plaque and the specific microbial composition of plaque may contribute to the transition from health to disease
-eliminating the disease-inducing stimulus, whether it is microbial, host, or environment, will help restore microbial homeostasis

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128
Q

Beneficial species of bacteria in the host: how do they affect the pathogenic spp?

A

1- passively occupying a niche
2- actively limiting a pathogen’s ability to adhere to appropriate tissue surfaces

3- adversely affecting the vitality or growth of pathogens

4- affecting the ability of a pathogen to produce virulence factors

5- degrading virulence factors produce by pathogens

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129
Q

Rads tend to over or under estimate the amount of bone loss?

A

Underestimate

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130
Q

Healing after periodontal therapy: regeneration

A

regeneration occurs thru growth from the same type of tissue that has been destroyed

131
Q

what replaces? 1-gingival epi 2- PDL

3-bone and cementum?

A

1- Epithelium
2- connective tissue

3- connective tissue (precursor of both), osteoblasts and cementoblasts

132
Q

Healing after periodontal therapy. Repair

A

simply restores the continuity of the diseased marginal gingiva and reestablishes a normal gingival sulcus

133
Q

Perio pocket healing, what is the result of healing by these cells? oral epithelium, gingival connective tissue, bone, and PDL

A

1- epi. result will be long junctional epithelium
2- C.T. result will be fibers parallel to the tooth surface and remodeling of the alveolar bone with no attachment to the cementum

3- Bone. root resorption and ankylosis

4- PDL, new formation of cementum and periodontal ligament!

134
Q

Action of power scalers, how does water play a role?

A

Acoustic streaming: unidirectional flow caused by ultrasound waves
Acoustic turbulence: created when the movement of the tip causes the coolant to accelerate, producing an intensified swirling effect

Cavitation: formation of bubbles in water caused by the high turbulence, bubbles implode and produce shock waves in the liquid

135
Q

Sonic units work at what frequency?

A

2000 to 6500 cycles per second and use a low or high speed air source from the dental unit
Tip travels in an elliptical or orbital stroke pattern

136
Q

Magnetostrictive ultrasonic devices work in what frequency range?

A

18,000 to 50,000 cycles per second

Vibrations travel from the metal stack to a connecting body that causes vibration of the working tip

137
Q

Piezoelectric ultrasonic units work in what frequency range?

A

18,000 to 50,000 cycles per second
ceramic disks in handpiece power the piezoelectric technology

Move in a linear pattern

138
Q

Tetracyclines

A

concentrates in periodontal tissues
-anticollagenase effects

  • bacteriostatic, effective against rapidly multiplying bacteria
  • more affective against gram-positive than gram-negative
  • high concentration in gingival crevice
139
Q

Metronidazole

A

bactericidal to anaerobic organisms and believed to disrupt bacterial DNA
-nitroimidazole compound

140
Q

Penicillins

A

-bactericidal! Inhibit bacterial cell wall production

141
Q

Amoxicillin

A
  • bactericidal
  • extended spectrum from penicillin, includes gram positive and negative

-susceptible to penicillinase (b-lactamase produced by bacteria that breaks up penicillin)

142
Q

Amoxicillin-Clavulanate Potassium

A

resistant to penicillinase

143
Q

Cephalosporin

A

Similar in structure and action to penicillins

-B-lactams

144
Q

Clindamycin

A
145
Q

Host modulation therapy: NSAIDS

A
  • inhibit prostaglandin formations (PGE2) which is produced by neutrophils, fibroblasts, macrophages, and epi cells in response to bacterial LPS
  • PGE2 upregulates bone resorption by osteoclasts and inhibits fibroblast fxn (which modulates immune response)

-Use has not taken off because of side effects

146
Q

Host modulation therapy: bisphosphonates

A
  • bone seeking agents that inhibit bone resorption by disrupting osteoclast activity
  • possess anticollagenase properties and interfere with osteoblast metabolism and secretion of lysosymal enzymes
  • unwanted effects include inhibiting bone calcification and inducing changes in WBC counts, also, avascular necrosis of jaws
  • none are currently being used
147
Q

Host modulation therapy: Sub-antimicrobial dose doxycycline

A
  • twice daily for up to 3 months, up to a max of 9 months

- exerts its effect by enzyme, cytokine, and osteoclast inhibition (not antibiotic!)

148
Q

Locally applied host modulation therapies

A

enamel matrix proteins
bone morphogenic proteins

growth factors

tetracyclines

149
Q

Maximum intercuspation definition (also centric occlusion)

A
  • position of mandible when there is maximum interdigitation and occlusal contacts b/w max and mand teeth
150
Q

Centric relation (Definition)

A

The position of the mandible when both condyle-disc assemblies are in their most superior position in their respective glenoid fossa and against the slope of the articular eminence of each respective temporal bone

151
Q

Gingival curettage vs subgingival curettage

A

Gingival= removal of the inflamed soft tissue lateral to the pocket wall and the junctional epi
Subgingival=performed apical to the junctional epi and severing the C.T. attachment down to the alveolar crest

*need to remove inflamed granulation tissue is questionable

152
Q

Curettage!

A
  • does not eliminate the causes of inflammation, so should always be proceeded by scaling and root planing
  • cutting edge is always against the tissue, inserted to engage the inner lining of the pocket wall and is carried along the soft tissue (usually horizontally)
  • ultrasonic instruments can do this with vibrations that disrupt tissue continuity
  • Excisional new attachment procedure=knife used to make internal bevel incision and remove tissue
153
Q

Healing after curettage

A

restoration and epithelialization of the sulcus require 2-7 days
-restoration of the junctional epithelium occurs in animals as early as 5 days after treatment

-immature collagen fibers appear within 21 days

154
Q

Apically displaced flaps

A

-advantage is preserving the outer portion of the pocket wall and transforming it into attached gingiva, so increases width of attached gingiva while eliminating pocket!

155
Q

Internal bevel incision benefits

A

1- removes pocket lining
2- conserves the relatively uninvolved outer surface of the gingiva

3-produces a sharp, thin flap margin for adaptation to the bone-tooth junction

156
Q

Modified Widman Flap

A

designed for exposing root surfaces and removal of pocket lining, not intended to reduce or eliminate pocket depth
-internal bevel incision, similar to envelope flap

-sling sutures used to close

157
Q

Undisplaced (unrepositioned) flap

A

improves accessibility for instrumentation and removes pocket wall, so reduces or eliminates pocket
-essentially an excisional procedure of the gingiva

  • commonly performed
  • internal bevel gingivectomy
158
Q

What # wall defect usually needs to be recontoured surgically?

A

one wall defects (sometimes two walls as well)

159
Q

Positive vs negative architecture

A 
Positive= radicular bone apical to the interdental bone
Negative= interdental bone more apical than the radicular bone
160
Q

Osteoinduction vs osteoconduction vs osteogenesis

A 
Induction= molecules in the graft (BMPs) convert the neighboring cells into osteoblasts which in turn form bone
Conduction= physical effect by which the matrix of the graft forms a scaffold that favors outside cells to penetrate the graft and form new bone

Genesis= formation of new bone by cells contained within the graft

161
Q

Demineralized freeze-dried bone grafts

A

demineralization in hydrochloric acid exposes the components of bone matrix, which are closely associated with collagen fibrils and have been termed bone morphogenic proteins (BMPs)

162
Q

BMPs

A

growth factor
-BMP-2, one of strongest bone producing varieties

  • induce diffentiation of mesenchymal stem cells to become bone producing osteoblast cells, so they are differentiation factors
  • binds tightly to collagen within minutes
163
Q

Enamel matrix proteins

A
  • purified enamel matrix proteins have been extracted from porcine developing enamel
  • use for perio tissue regeneration has been mixed
  • mainly amelogenin protein, which is secreted by hertwig’s root sheath and induce acellular cementum formation
  • EMDOGAIN- gel, mostly amelogenin

not osteoinductive, but osteopromotive (stimulates bone formation when combined with FDBA)

164
Q

Components of Gingival Crevicular Fluid

A
  • majority are enzymes
  • cellular elements
  • electrolytes (K, Na, Ca)
  • organic compounds (proteins, less than in serum) (Glucose, much higher (3-4x) than in serum)
165
Q

What are the cellular elements of GCF?

A

Bacteria
Desquamated epithelial cells

Leukocytes (migrate thru sulcular epithelium)

166
Q

Is protein content of GCF correlated to level of disease?

A

No

167
Q

Does GCF have cell or humoral immune responses?

A

BOTH

168
Q

The role of antibodies in gingival defense mechanisms is difficult to ascertain, but what is the consensus?

A

1- a reduction in antibody response is detrimental

2-antibody response plays a protective role

169
Q

The amount of GCF changes how in inflammation?

A

amount is greater when inflammation is present, and is sometimes proportional to the severity of infection

170
Q

What drugs have been shown to be excreted thru the GCF?

A

Tetracyclines, metronidazole

171
Q

Leukocytes in the dentogingival area?

A

Mostly PMNs
Are always present, even without disease

There are some mononuclear cells as well (58% B lymphocytes, 24% T, 18% phagocytes)- That is a higher ratio of T:B lymphocytes than in peripheral blood

-leukocytes are also found in saliva, and their main entry into the oral cavity is thru the sulcus

172
Q

Saliva!

What are the inorganic factors present in saliva that influence bacteria?

A

Ions and gases, bicarb, sodium, potassium, phosphates, calcium, flourides, ammonium, and carbon dioxide

173
Q

Saliva!

What are the organic components of saliva that influence bacteria?

A

Lysozyme, lactoferrin, myeloperoxidase, lactoperoxidase, and agglutinins (glycoproteins, mucins, macroglobulins, fibronectins, antibodies)

174
Q

What is lysozyme?

A

hydrolytic enzyme that cleaves the linkage between structural components of the glycopeptide muramic acid-containing region of the cell wall of certain bacteria in vitro
Works on both gram positive and negative!

175
Q

Myeloperoxidase?

A

enzyme similar to salivary peroxidase, released by leukocytes, bactericidal for actinobacillus

176
Q

Lactoperoxidase-thiocyanate system in saliva?

A

bactericidal to some strains of lactobacillus and streptococcus by preventing accumulation of lysine and glutamic acid

177
Q

What is the preponderant immunoglobulin found in saliva?

A

IgA (IgG is more prevalent in GCF)

178
Q

The major enzyme in saliva is?

A

Parotid amylase

179
Q

What is the most important salivary buffer in saliva?

A

Bicarbonate-carbonic acid system

180
Q

In clinically normal gingiva of humans, what is the basis of inflammatory cells?

A

Mostly T cells, very few B cells or plasma cells

181
Q

Stage 1 of gingivitis

A

Is subclinical
-vascular changes

-in response to microbial activation of resident leukocytes

182
Q

What determines how stage 1 gingivitis will progress?

A

The character and intensity of the host immune response (i.e., can it get back to a normal state, or will it progress to chronic inflammation)

183
Q

Stage 1 gingivitis, microscopic level changes

A

changes in blood vessels and adherence of neutrophils to bv walls (happens within 2 days to 1 week of plaque accumulation)
-Leukocytes migrate out of the vessels and are seen in increased quantities in the CT, junctional epi, and gingival sulcus

-exudation of fluid from gingival sulcus seen

184
Q

Stage 2 gingivitis (the early lesion)

A

evolves within about a week of plaque accumulation

-

185
Q

Microscopic changes with stage 2 gingivitis?

A

leukocyte infiltration in CT beneath junctional eli, consisting mainly of lymphocytes (T CELLS)
-junctional epi may begin to show development of rete pegs or ridges

  • collagen destruction increases (70% destroyed around the cellular infiltrate)- circular and dentogingival fibers appear to be most affected
  • PMNs release their lysosomes in association with the ingestion of bacteria
186
Q

Stage 3 gingivitis

Established lesion

A
  • Characterized by a predominance of plasma cells and B cells (IgG class)
  • Increased plasma cells differentiate this stage!
  • basal lamina destroyed in some areas
  • COllagen fibers destroyed
  • blood vessels become engorged and congested
187
Q

How do established gingivitis lesions progress?

A

Some remain stable and do not progress over months or years!

Some become more active and convert to destructive lesions

188
Q

Stage 4 gingivitis, or the advanced lesion, or phase of periodontal breakdown

A

fibrosis of gingiva and widespread manifestations of inflammatory and immunopathologic tissue damage
-plasma cells dominate CT and neutrophils dominate junctional epithelium

189
Q

What are the two earliest signs of gingival inflammation?

A

1-increased gingival crevicular fluid

2- bleeding from sulcus on gentle probing

190
Q

Histologic evaluations on animal specimens revealed that in early stages of gingivitis, what is ubiquitous?

A

expression of cytokines responsible for connective tissue breakdown (MMPs!)

191
Q

How does gingivitis differ in children vs adults?

A

Response in children is dominated by T cells (not B cells), very few plasma cells
Could explain why gingivitis in children rarely progresses to periodontitis

192
Q

Healthy gingiva is associated with what microorganisms?

And diseased gingiva?

A

1- mostly coccoid cells and straight rods

2- increased numbers of spirochetes and motile rods

193
Q

Pocket formation starts as?

A

inflammatory change in the ct wall of the gingival sulcus
-degeneration of ct due to cellular and fluid inflammatory exudate, and just apical to junctional epithelium, collagen fibers are destroyed

194
Q

what causes pain on probing of periodontal pockets?

A

ulceration of inner aspect of pocket wall

195
Q

What are two mechanisms associated with collagen loss?

A

1-collagenases and other enzymes secreted by vaious cells in healthy and inflamed tissue (such as fibroblasts, PMNs, macrophages)- these enzymes are called MMPs
2-fibroblasts phagocytize collagen fibers

196
Q

explain the gradual movement of the pocket

A

PMNs invade the coronal aspect of junctional epi due to inflammation, and once these occupy about 60%, the tissue detaches from the tooth surface. At the same time, as a result of collagen destruction, the apical cells of the junctional epi proliferate along the root, resulting in an apical shift

197
Q

Extension of junctional epi along the root requires?

A

healthy epithelial cells!

-If there is necrosis of the junctional epi, this impairs pocket formation and ulcerative gingivitis results

198
Q

Soft tissue wall of a periodontal pocket

A

C.T. edematous and densely infiltrated with plasma cells, lymphocytes, and PMNs. B.V.’s increased in number and are dilated and engorged. Necrotic foci are seen. Junctional epi at base of pocket in much shorter than a normal sulcus. Most severe degeneration is along the lateral wall of the pocket

199
Q

What are the different areas that can be seen within a periodontal pocket wall?

A

1-areas of relative quiescence
2-areas of bacterial accumulation

3-areas of emerging leukocytes

4-areas of leukocyte-bacterial interaction

5-areas of intense epithelial desquamation

6-areas of ulceration

7- areas of hemorrhage

200
Q

What predominates in an edematous pocket wall vs a fibrous pocket wall?

A

1-inflammatory fluid and cellular exudate predominate, wall is bluish red, soft, spongy, and friable
2- newly formed ct cells and fibers predominate, and the wall is more firm and pink

201
Q

What does the root surface look like in a periodontal pocket?

A
  • as pocket deepens, collagen fibers embedded in the cementum are destroyed and collagen becomes exposed to the oral environment
  • Sharpey’s fibers degenerate
  • becomes an environment favorable to bacteria penetration
  • viable bacteria have been found in 87% of the roots of periodontally diseased teeth!
  • can result in cementum breakdown and areas of necrotic cementum
202
Q

What is an area of increased mineralization in a periodontal pocket?

A

probably a result of an exchange, on exposure to the oral cavity, of minerals and organic components at the cementum-saliva interface
-SO, the mineral component of cementum increases (calcium, magnesium, phosphorus, fluoride)

-may offer increased resistance to decay

203
Q

Areas of demineralization?

A

often related to root caries

-root surface caries tend to progress around, rather than into, the tooth

204
Q

What is the dominant microoganism in root surface caries?

A

Actinomyces viscosus

205
Q

What zones are found at the bottom of a periodontal pocket?

A
  1. Cementum covered by calculus
  2. Attached plaque (covers calculus and extends apically, about 100 to 500 micrometers)
  3. Unattached plaque (extends apically to attached plaque)
  4. attachment of junctional epi to the tooth (in normal sulci is 500 micrometers, in pocket is reduced to 100 micrometers or so)
  5. semidestroyed connective tissue fibers- may be apical to junctional epi
206
Q

Microscopic differences in supraboney vs infraboney pockets

A
  • relationship of soft tissue wall of the pocket to alveolar bone
  • pattern of bone destruction

-direction of transseptal fibers of the PDL

207
Q

Micro-organisms that occupy periodontal abscesses are usually?

A

gram-negative anaerobic rods

208
Q

After inflammation reaches the boneby extension from the gingiva, what happens?

A

-it spreads to the marrow spaces and replaces the marrow with a leukocytic and fluid exudate, new blood vessels, and proliferating fibroblasts

209
Q

Where does resorption of the bone in periodontal disease begin?

A

In the marrow spaces, causing thinning of the surrounding bony trabecular and enlargement of the marrow spaces, followed by destruction of the bone and reduction in bone height

210
Q

Is bone destruction in periodontal disease a function of bone necrosis?

A

NO

It involves the activity of living cells along viable bone

211
Q

The amount of inflammatory infiltrate correlates with the degree of bone loss, but not with the number of ——-?

A

Osteoclasts!
However, the distance from the apical border of the inflammatory infiltrate to the alveolar bone crest correlates with both the number of osteoclasts on the alveolar crest and the total number of osteoclasts

212
Q

Microbiologically, periods of destructive activity in periodontal disease are associated with?

A

increase of the loose, unattached, motile, gram-negative, anaerobic pocket flora
Periods of remission have a dense, unattached, nonmotile, gram positive flora with a tendency to mineralize

Also, hypothesized that it goes from a T cell lesion to a predominantly B cell lesion

213
Q

How does bone destruction progress in periodontal disease?

A

bacterial plaque products induce the differentiation of bone progenitor cells into osteoclasts and stimulate gingival cells to release mediators that have the same effect
-Plaque products and inflammatory mediators can also directly inhibit osteoblasts

214
Q

What are the host factors released by inflammatory cells that play a role in periodontal disease?

A

Prostaglandins (and their precursers)
IL-1alpha, IL-beta

TNF-alpha

215
Q

What is buttressing bone formation?

A

areas of bone formation found immediately adjacent to sites of active bone resorption

216
Q

Central vs peripheral buttressing bone formation

A

Central- occurs within the jaw

Peripheral- occurs on the external surface

217
Q

How does the periodontium respond to an increase in the magnitude of occlusal forces?

A

With a widening of the PDL space, and an increase in the number and width of PDL fibers, and an increase in the density of alveolar bone

218
Q

What is more injurious to periodontium, constant or intermittent pressure?

A

CONSTANT

219
Q

What is the criterion that determines whether an occlusion is traumatic?

A

Whether it produces periodontal injury (not how the teeth occlude)

220
Q

What areas of the periodontium are most susceptible to injury from excessive occlusal force?

A

furcations

221
Q

Stage 1: injury
(stages of tissue response to increased occlusal forces)

1- If offending force is chronic, how does the ligament respond?

A

widened at the expense of the bone, resulting in angular bone defects without periodontal pockets, tooth becomes loose!

222
Q

Under forces of occlusion, tooth rotates around a fulcrum (or axis of rotation)
1-In single rooted teeth, this is where?

2- In multirooted teeth?

A

1- in the junction between the middle 1/3rd and apical 1/3rd

2- middle of the inter-radicular bone

223
Q

What does slightly excessive pressure cause?

How about greater pressure?

A

1- resorption of alveolar bone, widending of the PDL

2-compression of fibers, areas of hyalinization, areas of necrosis of the PDL; increased resorption of alveolar bone and resorption of the tooth surface occur

224
Q

What does slightly excessive tension cause?

Severe tension?

A

elongation of PDL fibers, apposition of alveolar bone, enlarged bv’s
2- widening of PDL, thrombosis, hemorrhage, tearing of the PDL, and resorption of bone

225
Q

What causes undermining resorption?

A

pressure severe enough to force the root against the bone

226
Q

Stage 2, repair (of trauma from occlusion)

A

when bone is resorbed by excessive occlusal forces, the body attempts to reinforce it with buttressing bone formation

227
Q

Stage 3, adaptive remodeling

-what happens to the PDL here IF the repair can’t keep up with the injury?

A
  • widened PDL, funnel shaped at crest, and angular defects in the bone, with no pocket formation
228
Q

What are the effects of insufficient occlusal forces?

What situations can cause it?

A

insufficient stimulation causes thinning of periodontal ligament
atrophy of fibers
osteoperosis of bone
reduction in bone height

hypofunction from open bite, lack of antagonistic tooth, unilateral chewing

229
Q

Does trauma from occlusion affect the gingiva?

A

No
Blood supply not affected to marginal gingiva

Does not cause pockets, gingivitis, or increase in GCF flow

230
Q

What bacteria are part of the red complex in people?

A

Tannerella forsythia
Treponema denticola

porphyromonus gingivalis

231
Q

The TMJ is formed by what bones?

A

the head of the mandibular condyle fits into the articular fossa of the temporal bone

232
Q

Centric relation is?

A

clinically determined relationship of the mandible to the maxilla when both condyle-disc assemblies are positioned in their most superior position in the maxillary fossa and against the slope of the articular eminence of the temporal bone

233
Q

The junctional epithelium is a unique epithelial entity in that it?

A

The surface cells are specialized for the purpose of attachment to the tooth, so there is no opportunity for sloughing! cells at basal layer instead just continually divide and move to within two or three cell layers of the tooth surface and migrate coronally, parallel to the tooth surface to eventually reach the floor of the sulcus and be sloughed into the gingival crevice

234
Q

ALSO, what are teh intercellular spaces like in junctional epi compared to other epithelium?

A

much greater, comprise about 18% of the volume of the epithelium, it’s “leaky”

235
Q

Connective tissue of the dentogingival complex? (type 1 and 3 fibers)- included are?

A

1- dentogingival fibers (from cementum to free and attached gingiva)
2-alveologingival fibers (extend from alveolar crest into free and attached gingiva)

3-circular fibers (wrap around tooth, maintain close adaptation of the free gingiva to the tooth)

4- dentoperiosteal fibers (from cementum, over alveolar crest, insert into alveolar process)

5- transseptal fibers (run interdentally, cementum to cementum, over the alveolar crest)

236
Q

Even in healthy gingiva, there are always what?

A

inflammatory cells, particularly neutrophils, also lymphocytes and macrophages

237
Q

Repeat, the initial lesion of gingivitis?

A

Slight elevation of vascular permeability and vasodilation
GCF flow out of sulcus

Migration of leukocytes (mostly neutrophils) thru the gingival ct, across the junctional epithelium, and into the sulcus

238
Q

Repeat, the early lesion of gingivitis?

A

Increased vascular permeability, GCF flow, vasodilation
large numbers of leukocytes infiltrating (mostly neutrophils, lymphocytes)

Degeneration of fibroblasts

Collagen destruction

Proliferation of junctional and sulcular epithelium into collagen-depleted areas

239
Q

Repeat, the established lesion of gingivitis?

A

dense inflammatory cell infiltrate (plasma cells, lymphocytes, neutrophils)
accumulation of inflammatory cells in ct

elevated release of MMPs and lysosomal contents from neutrophils

significant collagen depletion and epi proliferation

formation of pocket epithelium containing large numbers of neutrophils

240
Q

Repeat, the advanced gingivitis lesion

A

predominance of neutrophils in pocket epithelium
dense inflammatory cell infiltrate (mostly plasma cells)

apical migration of junctional eli

continued collagen breakdown

osteoclastic resorption of alveolar bone

241
Q

What are the predominant infiltrating cell types in the early lesion of gingivitis?

A

neutrophils and lymphocytes (mostly T cells)

242
Q

In the advanced lesion, what cells predominate in the pocket epithelium vs the connective tissues?

A

Pocket- neutrophils

CT- plasma cells

243
Q

Virulence factors come from both the host and the bacteria.

Microbial virulence factors are?

A

LPS
Bacterial enzymes and noxious products

microbial invasion

fimbriae

244
Q

Host-derived inflammatory mediators?

A

Cytokines
Prostaglandins

MMPs

245
Q

LPS
Lipopolysaccharides

Where are they found?

What do they act as?

How do immune systems in animals recognize these?

A

1-Outer membrane of gram-negative bacteria
2- endotoxins

3- TLR’s (toll-like receptors)

(porphyromonas gingivalis has an atypical form of LPS that is recognized by TLR2 and 4 (they are usually only recognized by 4)

246
Q

TLRs recognize what?

A

MAMPs (microbe-associated molecular patterns)

-causes an increase in production of inflammatory mediators and differentiation of immune cells

247
Q

LTA?

A

another component of gram-positive cell walls, lipoteichoic acid
Signals through TLR-2

248
Q

Some examples of bacterial enzymes and noxious products?

A 
NH3 (ammonia)
Hydrogen sulfide (h2S)

Short-chain carboxylic acids, such as butyric acid and proprionic acid

249
Q

What does butryic acid do?

A

induces apotosis in T-Cells, B-cells, fibroblasts, gingival epi cells

250
Q

Plaque bacteria also produce what? that causes tissue breakdown of the periodontium

A

Proteases

251
Q

Host response: cytokines

A

These bind to cell surface receptors, trigger a sequence of intracellular events that lead ultimately to the production of protein by the target cell, which alters that cell’s behavior

252
Q

What cell types produce cytokines?

A

large number, including inflammatory cells, as well as resident cells in the periodontium (fibroblasts, epi cells)

253
Q

How can cytokines mediate connective tissue and alveolar bone destruction?

A

by the induction of fibroblasts and osteoclasts to produce MMPs

254
Q

What are the most important cytokines in periodontal disease?

A

IL-1Beta

TNF-alpha

255
Q

Prostaglandins

These are?

A

1-a group of lipid compounds derived from arachidonic acid

2- Arachidonic acid is metabolized by COX-1 and 2 to generate a series of prostanoids (which includes prostaglandins)

256
Q

What does PGE2 result in?

A

vasodilation and induces cytokine production

257
Q

COX2 is upregulated by?

A

IL-1B, TNF-alpha, and bacterial LPS

258
Q

What specifically does PGE2 result in?

A

induction of MMPs and osteoclastic bone resorption, major role in tissue damage!

259
Q

What cells produce MMPs?

A

variety, neutro, macro, fibroblasts, epi cells, osteo blasts and calsts

260
Q

What do MMPs degrade?

A

Collagen, gelatin, elastin

261
Q

MMPs are secreted in what form?
And what activates them?

What produces the activation factor?

A

1- Latent
2-proteolytic cleavage by proteases (such as cathepsin G)

3- Neutrophils

262
Q

What are some key inhibitors of MMP?

A

proteinase inhibitors such as glycoprotein alpha1-antitrypsin and alpha2-macroglobulin (large plasma protein produced by the liver)

263
Q

What effect do tetracyclines have on MMPs?

A

inhibitory!

264
Q

IL-1Beta

What antagonizes IL-1Beta

A

key role in inflammation, innate immune response
2- PGE2, platelet-activating factor, nitrous oxide

Plays a big role in the pathogenesis of periodontal disease!

3- IL-1Ra

(IL-18 might also play a large role in perio dz)

265
Q

TNF-alpha

along with IL-1B is a big player in perio

A

Induces MMP secretion! (IL-1B doesn’t)
Less potent affect on osteoclasts than IL-1B

Secreted particularly by macrophages in response to LPS

266
Q

IL-6

A

Also plays a big role in perio, but not as big as IL-1B and TNF-a
Stimulated by cytokines like the above

267
Q

What are the cells mainly responsible for PGE2 production?

A

Macrophages and fibroblasts

268
Q

What effects does PGE2 have?

A

Contributes signficantly to bone loss

Induces secretion of MMPs and osteoclastic bone resorption

269
Q

In healthy tissues, MMPs are mainly produced by?

A

fibroblasts

270
Q

What are TIMPS?

A

Tissue inhibitors of metalloproteinases

271
Q

What are the predominant MMPs in periodontal diease?

A

MMP-8 and MMP-9
Secreted by neutrophils

Very effective at degrading type 1 collagen (most abundant type in periodontal ligament)

272
Q

MMP and bone destruction? expressed by?

A

osteoclasts

cathepsin K is a protease that also plays a role in bone destruction

273
Q

What antimicrobial peptides are expressed by epi cells? (making them an important part of innate immunity?)

A

Defensins

Epi cells also secrete chemokines to attract neutrophils

274
Q

What bad things do neutrophils do?

A

Release large quantities of MMPs and other destructive enzymes

275
Q

Bone resorption ceases when there is what distance between sites of bacteria in the pocket and bone?

And bone resorbs so that there is always a width of noninfiltrated ct of —– overlying the bone?

A
  1. 5 mm

0. 5 mm

276
Q

What two critical factors determine whether bone loss occurs?

A

concentration of inflammatory mediatros in the gingival tissues must be sufficient to activate pathways that lead to bone resorption

Inflammatory mediators must penetrate to within a critical distance of the alveolar bone

277
Q

What regulates the expression of RANKL and OPG?

A

IL-1beta
TNF-alpha

  • T cells express RANKL
  • In periodontitis, there is increased levels of IL-1b and TNF-a and increasing numbers of T-cells
278
Q

What resolves inflammation?

A

Lipoxins, resolvins, protectins

279
Q

Lipoxins1- Their presence indicates?
2- They are derived from?
3-They inhibit what?
4- They signal macrophages to do what?

A

1- resolution of inflammation2- arachidonic acid, they are eicosanoids
3- neutrophil chemotaxis, recruitment, and adhesion
4- phagocytose the remnants of apototic cells without generating an inflammatory response

280
Q

Resolvins1- derived from?
2- their effects are?
They are highly potent!!!

A

1- omega 3 fatty acids, eicosapentaenoic and docosahexaenoic acids2- Inhibit neutrophil infiltration and transmigration, inhibit production of proinflammatory mediators, and have potent anti-inflammatory and immunoregulatory effects

281
Q

Infection of host cells by P. Gingivalis involves?2- It is initiated through what?

A

1- the action of proteases and cell surface fimbriae2- thru signalling via interaction of bacterial components with surface integrins, PAR1 and 2, and TLR

282
Q

P. Gingivalis has also been shown to be able to migrate thru the basement membrane of epithelial layers and invade connective tissue

A

facilitated by bacterial-derived proteases and host proteases derived from infiltrating neutrophils

283
Q

What do epithelial cells produce and secrete in response to periodontal bacteria?

A

MMPsrange of cytokines (IL-1B, TNF-a, IL-6)…

284
Q

Sentinel cells of the immune system that are stimulated with periodontal bacteria include?

A

Macrophages and dendritic cells, which express and PRR, which interact with MAMPs of bacteria and signal immune responses

285
Q

The interaction of what adhesion molecules on endothelial and epithelial cells with ___ on neutrophils facilitates neutrophil migration?

A

1- ICAM-1 and LFA-32- Beta 2 integrins

286
Q

The distribution of leukocytes in periodontal disease is not even. ____ predominate in the connective tissue and ______ in the sulcus

A

1- mononuclear cells2- Neutrophils

287
Q

The clinical ebb and flow of periodontal disease is a reflection of fluctuations in ?

A

Adaptive immunity

288
Q

What are antigen presenting cells?

A

Cells that take up microbes and their antigens, then migrate to lymph nodes and interact with T cells to present antigen; They include B cells, macrophages, and at least 2 types of dendritic cells (langerhans, dermal)They express MHC class II molecules ncessary for antigen presentation (MHC expression might be induced in other cells of the periodontium as well)

289
Q

What is the predominant phenotype of T cells in the stable periodontal lesion?And what happens as the lesion worsens?

A

CD4+ helperMay lead to a progression towards a destructive, B cell dominated lesion

290
Q

Antibodies1- What produces them?
2- Which antibodies are found most common in perio?
3- Are they helpful/hurtful

A

1- B cells. These antibodies seem to have high titer but low biologic activity. High levels of plasma cells also are seen with high levels of antibodies2- IgG (few IgM and IgA)
3- Unknown. Sometimes can lead to production of autoantibodies which may contribute to destruction?

291
Q

What aspect of immunity potentially can explain the fluctuations noted in periodontal disease?

A

The interaction between T helper cells (Th1 and Th2)Definitive evidence for this is lacking

292
Q

What are the major inorganic components of calculus?

A

Calcium phosphate, calcium carbonate, magnesium phosphate

293
Q

What two types of crystals are also typically found in calculus

A

Hydroxyapetite, octacalcium phosphate

294
Q

What does the organic component of calculus consist of?

A

Protein-polysacchardie complexes, desquamated epithelial cells, leukocytes, and various micro-organisms

295
Q

what are the differences between supra and subgingival plaque?

A

Ratio of calcium to phosphate is higher subgingivallySodium content increases with pocket depth

296
Q

What is the main source of minerals for supragingival vs subgingival calculus?

A

Supra- salivaSub- GCF

297
Q

which is potentially more important in calculus formation, phosphorus or calcium?

A

Phosphorous

298
Q

Dental plaque is composed primarily of ?

A

Microorganisms

299
Q

In supragingival plaque, what bacteria predominate at the tooth surface vs. the outer surface of the plaque mass?

A

Gram-positive cocci and short rods (surface)

Gram-negative rods and filaments (spriochetes), outer surface

300
Q

Three phases of plaque formation?

A

1- pellicle formation, organic material, acquired, happens within 1 minute of cleaning, bacteria attach to this, not to the tooth directly
2- adhesion of bacteria

3- colonization and plaque maturation

301
Q

What determines if bacteria will adhere to a pellicle?

A

specific interactions b/w microbial cell surface “adhesin” molecules and receptors in the salivary pellicle (only a small proportion of oral bacteria will fit this)

302
Q

What is coadhesion? What does this lead to?

A

Primary colonizers adhered to the tooth surface provide new receptors for attachment by other bacteriaMicrocolonies and eventually to a mature biofilm

303
Q

Is bacterial growth faster in old or new plaque?

A

Faster in new, nutrients become limited as the plaque biomass grows

304
Q

How much more resistant are organisms in a biofilm than in their planktonic state?

A

1000 to 1500 times

305
Q

What is the ecologic plaque hypothesis?

A

total amount of dental plaque and the specific microbial composition of plaque may contribute to health and disease (mix of specific plaque hypothesis and nonspecific…)

306
Q

Periodontitis is considered a mixed infection; treatment with antibiotics?

A

Difficult because not all periodontopathogens are equally susceptible to the same antibiotic

307
Q

recent microbiologic tests indicated that the presence of periodontopathogens alone is not sufficient for the development of periodontitis; several of these pathogens have been identified in disease free patients

A

So the specificity (presence of a pathogen means periodontitis) of microbial detection is very low; so the understanding of etiology is complicated; threshold level between health and disease is unknown and different between different individuals

308
Q

Does periodontitis fit into Koch’s postulates? (bacteria routinely isolated from diseased individuals; grown in pure culture in the lab; produces a similar disease when put into others; be recovered from the same disease in lab animals)

A

No, primary problems being the inability to culture all the organisms that have been associated with the disease, the lack of a good animal model to study periodontitis, and the difficulties inherent in defining and culturing sites of active disease

309
Q

Allogenic vs autogenic succession? (change in bacterial community)

A

Allogenic- change in the composition of a bacterial community as the result of external, nonmicrobial factors (ex: smoking)Autogenic- interbacterial and viral-bacterial interactions are involved

310
Q

The current concept concerning the etiology of periodontal disease considers 3 groups of factors that determine whether active periodontal destruction will occur in a subject: what are they?

A

1- susceptible host2- presence of pathogenic spp.

3- absence/small proportion of so-called beneficial bacteria

311
Q

Comparing the microbiota b/w health, gingivitis, and periodontitis, what microbial shifts can be identified as health progressed to periodontitis?

A

1- From facultative anaerobes to obligate anaerobes2- From nonmotile to motile
3- From cocci to rods
4- From gram-positive to gram-negative
5- from fermenting to proteolytic species

312
Q

What are gingipains?

A

enzymes responsible for at least 85% of the total host protein degradation activity (They are tissue destructive enzymes released by bacteria)

313
Q

What is direct recognition of microbes by the host mediated by?

A

By the recognition of MAMPs by Pattern-recognition receptors (PRRs)

314
Q

How long does it take for adative immunity to have an adequate cellular or humoral response?

A

7 to 10 days

315
Q

What are critical for recognition of microbes by the innate immune system and for bridging innate and adaptive immune responses?

A

TLRs (these are PRRs)

316
Q

What IL is likely involved in the tolerance of commensal bacteria?

A

IL-8 (not released in response to commensals)

317
Q

Are epithelial cells equipped with PRRs?

A

YES, they respond to MAMPs by secreting various cytokines and chemokines (IL-8, antimicrobial peptides)

318
Q

Expression of Th1-type cytokines has been associated with _____, whereas Th2 cytokines were found in higher levels in _______-affected tissues

A

1- gingivitis

2- Periodontitis

319
Q

RANKL, produced by? (involved in osteoclast differentiation, survival, activation)

A

fibroblasts, osteoblasts, chondrocytes, mesenchymal cells, T and B cells

320
Q

OPG- decoy receptor of RANKL- secreted by?

A

osteoblastic cells, bone marrow stromal cells, fibroblasts

321
Q

Patients with periodontal disease have higher levels of?

A

RANKL, lower levels of OPG

322
Q

The increased susceptibility of diabetic patients to infection has been hypothesized as being due to?

A

PMN deficiencies

323
Q

How do systemically administered steroids hinder healing?

A

depressing inflammatory reaction, inhibits growth of fibroblasts and the production of collagen, and the formation of endothelial cells

Jane (and Margie)'s Veterinary Dentistry export questions (17 decks)

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