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perio final Flashcards

1
Q

support and contour of free ging

attaches encircles tooth at the “neck”

A

Circular gingival fiber

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2
Q

support of gingiva

attaches gingiva to cementum

A

Dentogingival

Dento=cementum

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3
Q

Anchors tooth to bone

attaches cementum to periosteum

A

dentoperiosteal

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4
Q

attaches gingiva to the bone (periosteum)

A

alveologingival

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5
Q

keeps teeth in alignment, protects interprox bone , connect teeth

A

Transseptal (interdental)

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6
Q
  • Many cells
  • Little extracellular matrix
  • Internal/external basal lamina
  • No blood supply
A

Gingival Epithelial Tissues

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7
Q
  • Few cells
  • Mostly extracellular matrix
  • Strongropelikefibers
  • Rich blood supply
A

Gingival Connective Tissue (Lamina Propria)

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8
Q
  • Cementum
  • Dentin
  • Alveolar bone
  • Pulp
  • Not enamel – this is epithelial tissue
A
  • Cementum
  • Dentin
  • Alveolar bone • Pulp
  • Not enamel – this is epithelial tissue
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9
Q
  • Fibroblasts
  • Cementoblasts
  • Osteoblasts
A

(makes collagen)
(makes cementum)
(makes bone)

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10
Q
  • Cell-to-cell connection
  • Two neighboring epithelial cells together
  • Found in gingival epithelium
  • Like snap closure on a jacket
A

Desmosome

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11
Q

Originates from the cementum and runs apically to insert into the alveolar crest.
Resists lateral movement of the tooth and keeps tooth in its socket.
The first fibers to be formed before tooth eruption has occurred

A

Alveolar crest

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12
Q
  • Collagen fibers from the PDL
  • Insertion into cementum & alveolar bone
  • Inserts into the hard tissues at 90 degrees
  • The angulation increases its strength
A

Sharpey’s Fibers

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13
Q

Originates from cementum and runs at right angles and inserts into bone.
Opposes lateral forces.
The second fibers to be formed as soon as the first tooth-to-tooth contact has occurred

A

Horizontal

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14
Q

Found in the middle third of the root api to the horizontal fibers; originates from cementum and runs coronally and diagonally into bone.
Absorbs occlusal forces.The most abundant and thus the principal attachment of the tooth.

A

Oblique

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15
Q

Originates from cementum of the apex of the root, spreading out apically and laterally into bone.
Resists tipping of the tooth.
One of the last fibers to form.

A

Apical

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16
Q

From the crest of the interradicular septum extending to the cementum in the furcation area.
Resists the forces of luxation (pulling out) and tipping.
.Lost when bone is destroyed in the furcation area in disease.

A

Interradicular

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17
Q
  • Connect epithelial cell to basal lamina connection

* Found in gingival epithelium

A

Hemidesmosome

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18
Q

Base of the sulcus
Joins gingiva to the tooth
• Nonkeratinized
• Similar to SE, it is vulnerable.
• More permeable than the OE or SE
• Attaches the gingiva enamel and/or cementum
• JE provides a seal at the base of the pocket
• JE also is a protective barrier
• Between the plaque biofilm and the underlying
connective tissue
• High rate of cell turnover

A

JunctionalEpithelium(JE)

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19
Q
  • Cover outer surface of Free & Attached gingiva
  • From the crest of the GM to MGJ
  • Wavy boundary junction with the connective tissue (in health)
  • Epithelialridgesconnectwiththecollagenfibersinthe connective tissue
  • May be keratinized or parakeratinized
A

Oral Epithelium (OE)

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20
Q
  • Lining of the sulcus
  • Thin and nonkeratinized
  • Vulnerable to stresses
  • Junction to the connective tissue is smooth
  • Permeable, allows fluid flow à GCF
A

Sulcular Epithelium (SE)

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21
Q

Connective tissue attachment + Junctional Epithelium
CT (1.07mm) + JE (0.97mm) =
• Important when fabricating restorations
• It must not invade this

A

Biologic Width
BW (2.04mm)
Should be at least 3mm on a radiograph only!

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22
Q

Loss of radicular bone including marginal bone

A

Dehiscence

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23
Q

• Loss of radicular bone but not marginal bone
VS

• A “window” of bone resorbed on radicular surface

A

Dehiscence

Fenestration

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24
Q
  • Forms before tooth eruption
  • No cementocytes
  • Covers coronal half to 2/3 of root • Thinnest at CEJ
  • Mostly Sharpey fibers
  • Thickness 30 – 60 μm
A

Acellular

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25
Q 
At apical 1/3 
• Forms faster than acellular 
• Has cementocytes 
• Continues to form after tooth eruption 
• Less calcified
• Thickness 150 – 200 μm
A

Cellular

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26
Q
  • Forms before tooth eruption
  • No cementocytes
  • Covers coronal half to 2/3 of root • Thinnest at CEJ
  • Mostly Sharpey fibers
  • Thickness 30 – 60 μm
A

Acellular cementum

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27
Q 
the cementum At apical 1/3 
• Forms faster than acellular 
• Has cementocytes 
• Continues to form after tooth eruption 
• Less calcified
• Thickness 150 – 200 μm
A

Cellular cementum

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28
Q

• Three microscopic interfaces @ CEJ

  1. Overlap
  2. Meet
  3. Gap
A

60%
30%
10%

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29
Q

• cells that do removal of mineralized material and organic matrix of bone

A
  • Osteoclasts:

* C = “Consume”

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30
Q

• creation of bone matrix

A
  • Osteoblasts:

* B = “Build”

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31
Q
  • CN V: Trigeminal nerve
  • Division II –
  • Division III –
A

to the maxilla
• Afferent
to the mandible
• Afferent & Efferent

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32
Q

• Spongy
• Lattice-like
• Between Cortical bone & Alveolar bone proper
Formed around tooth to form support for the Alveolar bone proper

A

Cancellous Bone

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33
Q 
• Hard outer wall of jaws
• On facial & lingual aspects 
	• Surrounds alveolar bone proper 
	• Gives support to socket 
	• Not radiographically seen 
	• Alveolar crest most coronal part of this 
Cortical bone
A

Cortical bone

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34
Q

measured from a fixed point—the CEJ—to the base of the sulcus or periodontal pocket
Refers to the position of the attached periodontal tissue at the base of the pocket or sulcus

A

Clinical Attachment Level (CAL)

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35
Q

measured from the gingival margin to the base of the sulcus or periodontal pocket

A

probing depths

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36
Q

Long-lived, out of control inflammatory response
• Continues for more than few weeks
• Destroy healthy tissue and cause more damage than the original problem – overzealous immune system
• Classic warning signs are absent
• Problems go unnoticed by patient • Clinically, pain is often absent

A

Chronic Inflammation

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37
Q
  • Short-term & normal process
  • Increased movement of plasma and leukocytes from the blood to injured tissues
  • Shows five classic signs of acute inflammation
    1. Heat
    2. Redness
    3. Swelling
    4. Pain
    5. Loss of function
A

Acute Inflammation

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38
Q

Body sends host defense components to site of infection

In an attempt to heal and eliminate pathogens

A

Inflammatory Response

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39
Q

• Within minutes after cleaning, acquired pellicle forms over tooth surface
• Acquired pellicle composed of salivary glycoproteins
Allows for free-flowing microbes to stick to the pellicle

A

Stage 1: Initial Attachment

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40
Q

What stage:

  • Microbes able to withstand hydrodynamic forces
  • Predominantly gram + cocci
  • Attains permanent attachment
  • Attached microbes produce substances to attract others
  • Coaggregation
  • When genetically different bacteria become attached to one another
A

Stage 2: Permanent Attachment

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41
Q
  • Self-protective matrix formation
  • Firmly attached bacteria secrete protective matrix -Extracellular protective matrix
  • Consists of proteins, glycolipids, and bacterial DNA
  • Protected against host immune response
  • Chronic disease established
A

Stage 3: Maturation Phase I

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42
Q
  • Mushroom shape microcolonies form
  • Attached to the tooth by a narrow base
  • Specific species grow at an accelerated rate
  • Biofilm becomes thicker, forming on top of each other
  • Fluid channels form within the matrix
  • Carries nutrients to the microbes & disposes waste
  • Cell to cell communication occurs among each other
A

Stage 4: Maturation Phase II

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43
Q

what Stage of biofilm

Microbes disperse from colony to spread to other surfaces

A

Stage 5: Dispersion

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44
Q

Condition in which a purulent oozes from the gingival surface when pressed.

A

gingival suppuration

pus

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45
Q 
recession = + 
Enlargement= -
A

Determining attachment loss and inflammation

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46
Q

Recession that dosnt extend to the mucogingival junction with no periodontal bone loss in the interdental areas

A

Millers class 1

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47
Q

Recession that extends to/ beyond the mucogingival junction/ no interdental bone loss

A

Millers class 2

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48
Q

Recession extends to beyond the mucogingival junction, with some periodontal attachment loss in the interdental area or malpositioning of the teeth

A

Millers class 3

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49
Q

Recession that extends to or beyond mucogingival junction with severe bone loss and soft tissue loss interdentally/ with malpositioning of teeth

A

class 4

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50
Q

process whereby microorganisms irreversibly attach to and grow on a surface and produce extracellular polymers that facilitate attachment and matrix formation.

A

Biofilm formation

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51
Q

• Present @ birth
• Not antigen specific
Does NOT improve with repeated exposure to pathogen

A

• Innate

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52
Q

• Develops throughout life
• Antigen specific
• Lag time between infection and response
• Memory develops which may provide lifelong
immunity to reinfection

A

• Adaptive

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53
Q

to defend the life of the individual by identifying foreign substances in the body and developing a defense against them.

A

Prime Purpose of Immune System

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54
Q
  • Also called neutrophils
  • Rapid responders
  • 1st line of defense against infection
  • Capture & destroy
  • Short-lives (dies after engorged with bacteria)
  • Attracted to bacteria by chemotaxis
  • Digests bacteria by using lysosomes
  • Perio pathogens most effectively destroyed by PMNs
A

PMN

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55
Q
  • when in bloodstream =?
  • when in tissues =?
  • Slower to arrive than PMNs
  • Surround & destroy bacteria
  • Long-lives, seen in chronic inflammation
A

Monocytes

Macrophage

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56
Q

Antibodies

Otherwise known as immunoglobulins (Ig)

Five major classes IgM

A

IgD
IgG
IgA: found in saliva!
IgE

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57
Q

part of the body’s immune system. They help the body fight infection and other diseases.

A

White blood cells (WBC)
Types of white blood cells are granulocytes (neutrophils, eosinophils, and basophils), monocytes, and lymphocytes (T cells and B cells).

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58
Q

• Small, and they reorganize & control invaders

A

Lymphocytes

WBC

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59
Q 
when in bloodstream 
when in tissues 
• Slower to arrive than PMNs 
• Surround & destroy bacteria 
• Long-lives, seen in chronic inflammation
A
  • Monocyte:

- Macrophage:

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60
Q

-Makes antibodies and releases them into bloodstream

Y-shaped proteins that bind

A

B-Lymphocytes (B-Cells)

One end to antigen, other to B-Cell
Helps B-cell kill antigen 
Can change to two types of B-Cells: 
Plasma B-Cells
Memory B-Cells
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61
Q

Intensifies the response of the B cells and the macrophages to the bacterial invasion.

This further stimulate immune response

A

T-Lymphocytes (T-Cells)

T-cells produce cytokines

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62
Q

….travel via bloodstream

  1. Near the infection site, ….push their way between the thin layer of epithelial cells and enter the connective tissue (extravasation)
  2. This process = transendothelial migration
A

Migration of Leukocytes to Infection Site

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63
Q

• Process where leukocytes
1. Enter the connective tissue
2. Are attracted to the infection site
• Because of biochemical compounds released by invaders

A

Chemotaxis

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64
Q

process by which a cell uses its plasma membrane to engulf a large particle, giving rise to an internal compartment

A

Phagocytosis

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65
Q

Which inflammatory process?

  1. Blood vessels in infection site become more permeable
  2. PMNs arrive first at site
  3. PMNs release cytokines to facilitate response
  4. Liver produces C-reactive proteins (CRP)
  5. If body succeeds in getting rid of infection, tissue will heal, immune cells leave area with no damage to tissues
A

Acute Inflammatory Process

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66
Q

• Dysfunction of the resolution pathway which is supposed to shut down the inflammatory response after initial response
• Result:
1. Perio tissues do not heal
2. Chronic, progressive and destructive, nonresolving inflammation

A

Periodontal Disease

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67
Q

Signs and symptoms during chronic inflammation may disappear entirely or partially during period of remission

A

Remission •

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68
Q

• Signs and symptoms may recur with all of their severity in an active period called exacerbation

A

• Exacerbation

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69
Q
  • Initial lesion
  • Early lesion
  • Established lesion
  • Advanced lesion
A

4 Histologic Stages in Periodontal Disease Development

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70
Q

What stage?
Bacteria colonize near GM: initial location of biofilm
• GCF increases in volume as response to bacteria presence
• Vascular dilation à PMN migration
• Clinically, tissue looks healthy
• Host response by PMNs successful if most bacteria is destroyed
• Body can repair any damage at this point
• If bacteria is not controlled, early gingivitis develops

A

Initial Lesion: Bacterial Accumulation

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71
Q
  • Biofilm matures, bacterial toxins penetrate the JE
  • Increase vasculature/permeability, more PMNs move in
  • PMNs release cytokines that cause localized destruction of CT
  • Macrophages recruited at this point, release more cytokines
  • Clinically: edema and redness at GM seen
  • Initiation of good self-care can disrupt biofilm for complete health to return
  • IF immune system fails to shut off this host response à lesion progresses to established gingivitis
A

Early Lesion: Early Gingivitis

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72
Q

What stage of gingivitis ?
• Biofilm extends subgingivally
• Disrupts attachment of the most coronal of the JE attachment
• More stimulation of the immune system
• More PMNs, macrophages, and lymphocytes
• Plasma cells now produce large # of antibodies to assist
• This host response end up getting healthy CT destroyed
• JE loses attachment to root surface and transforms into pocket epithelium which is thinner & more permeable

A

Established Lesion: Established Gingivitis

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73
Q

Clinically all features of gingivitis are accentuated
• Good self-care vital at this point to reverse destruction
• In some pts, if bacterial infection not controlled à periodontitis

A

Established Lesion: Established Gingivitis continued

74
Q

Biofilm spreads laterally as well as apically along the root
• Chronic inflammation causes harm on periodontium
• PMNs & macrophages cause destruction of CT and PDL
• Macrophages produce byproducts that destroy alveolar bone
• Gingival pocket à Periodontal pocket
• Destruction caused by host response overwhelms any tissue repair attempt
• Clinically, periodontal pocket detected, bone loss, furcation involvement, possible mobility depending on extent
• Changes are irreversible

A

Advanced Lesion: Periodontitis

75
Q
  • Changes in color, contour, and consistency of gingival tissues
    • Can be observed clinically
  • 4-14 days after biofilm accumulation in sulcus
A

Gingivitis

Progression of Gingivitis 
• Tissue damage is reversible
 • Body can repair the damage 
• Gingivitis can persist without progressing into periodontitis! 
• This depends on the person
76
Q

Acute vs. Chronic Gingivitis

A
  • Acute gingivitis
  • Lasts for short period of time
  • Tissues appears swollen
  • Due to fluid in the gingival connective tissues
  • Chronic gingivitis
  • Lasts for longeràmonths or years!
  • Can result in more fibrotic tissue
77
Q 
• JE located belownormal (apically) 
	• SE of pocket thickens 
	• Small SE ulcerations expose inflamed 
underlying CT 
	• Collagen destruction in area of inflammation 
	• Alveolar bone destruction 
	• Permanent destruction of PDL 
Cementum becomes exposed to the biofilm
A 
Periodontitis 
 Characteristics
• Apical migration of JE 
• Loss of connective tidsue
• Loss of alveolar bone
• Tissue damage irreversible v
78
Q
  • Inflammation spreading:
  • Into gingival CT
  • Into the alveolar bone
  • Into the PDL
  • Inflammation spreads like this because it’s the path of least resistance
  • Usually results in suprabony perio pocket
A

Horizontal Bone Loss Pathway

79
Q

Inflammation spreading:
• Into gingival CT
• DIRECTLY into PDL space
• Into alveolar bone
• Occurs when crestal PDL are weak and no longer act as an effective barrier against inflammation
• Usually results in an infrabony perio pocket

A

Vertical Bone Loss Pathway

80
Q

• Bowl-shaped defect in interdental bone
• The picture is showing how a crater is affecting roots of two adjacent teeth
• Craters can happen in only one tooth as well
Results in difficulty in cleaning interdental surfaces

A

Osseous Crater

81
Q

• Site that shows continued destruction

• Site that shows stable attachment over a period of time
Probing depths & radiographs only show past destruction

A
  • Active disease site

* Inactive disease site

82
Q

a periodontal pocket in which the bottom is coronal to the underlying bone.

A

suprabony pocket

horizontal bone loss

83
Q

a periodontal pocket in which the bottom is apical to the level of the adjacent alveolar bone.

A

infrabony pocket

vertical bone loss

84
Q

Periodontal Health

A
  • Free from inflammatory perio disease
  • Absence of symptoms such as:
  • BOP
  • Erythema
  • Edema
  • Symptoms
  • Attachment loss
  • Bone loss
85
Q

Periodontal health on an intact periodontium

A

healthy

86
Q

Periodontal health on a reduced periodontium in a nonperiodontal patient

A

Clinical gingival health on a reduced periodontium is characterized by an absence of bleeding on probing, erythema, edema and patient symptoms in the presence of reduced clinical attachment and bone levels.

87
Q
  • No loss of perio tissue (past or present) =?

* Past hx of reduced perio tissue but no current activity of =?

A

Intact periodontium

Reduced periodontium

88
Q

• Return of periodontitis that was previously arrested
• Anyone with prior hx is at risk
Happens especially with noncompliant pt

A

• Recurrent

89
Q
  • Return of periodontitis but with an unknown etioogy
  • Happens despite:
  • Good home care
  • Compliant to recommendations
A

• Refractory

Tx for Refractory Periodontal Disease 
• Review OH
• SRP
• Systemic or local antibiotics
 • Removal of hopeless teeth 
• Correcting local factors
• Surgery
• Frequent maintenance
90
Q
  • Necrosis of the gingival tissues, PDL and alveolar bone
  • Rapidly escalates & produce periodontal attachment loss within days
  • Involved interdental areas separated into one facial papilla and one lingual papilla with necrotic depression between them
  • Craters formed with the separation
  • Once craters are formed, PDL and Bone become destroyed
A

Necrotizing Periodontitis (NP)
Other Names of NPD
• Trench mouth
• Acute necrotizing ulcerative gingivitis (ANUG)
• Necrotizing ulcerative gingivostomatitis

91
Q

• Limited to gingival tissues • No bone loss

A

Necrotizing Gingivitis (NG)

92
Q

• Rare and most extensive of NPD
• Associated with severe immunocompromised med system
• Most distinguishable feature:
• Bone denudation extending to alveolar mucosa
• May result in oral-antral fistula & osteitis (inflammation of bone)
• Immediate consult to oral pathologist, OMFS, and physician
• Severe necrosis
• Extends beyond gingiva to other parts of the oral cavity:
tongue, cheeks, palate

Most severe and rarest among the necrotizing perio disease

A

Necrotizing Stomatitis

93
Q

Initial Appointment
• Comprehensive medical hx
• Gentle removal of pseudomembrane with cotton pellets
• Limited supragingival instrumentation
• Stay supragingival, preferably with ultrasonic instrument
• May need topical anesthesia
• Subgingival instrumentation can extend the infection!
• Chlorhexidine rinse 2x daily or hydrogen peroxide:water (1:1) every 2-3 hrs for few days
• Analgesic such as NSAID (ibuprofen) for pain relief
• Advise to return in about 2 days for a checkup of the symptoms
• Tell pt that tx is not complete when the pain stops

A

Treatment of Necrotizing Gingivitis: 1st Visit

94
Q
  • 2nd Appointment (about 2 days after 1st visit)
  • Subgingival instrumentation usually can be started
  • Pay attention to systemic symptoms
  • Encourage continued self-care
  • Smokingcessation
  • Stress reduction
  • Nutrition
A

Treatment of Necrotizing Gingivitis: 2nd Visit

95
Q
  • Third appointment (about 5 days after initial appointment)
  • Patient should be symptom free
  • Complete subgingival instrumentation
  • Further pt self-care counseling
  • Depending on systemic symptoms, antibiotics may be necessary
  • Make appt for comprehensive clinical assessment
  • Toaddressanypossibleunderlyingperiodisease
  • Pt needs to be reevaluated in about 1 month
A

Treatment of Necrotizing Gingivitis: 3rd Visit

96
Q

Acute =?

Chronic =?

A

A=Rapid, painful, lack of spontaneous draining

C= Slow, may not feel, sinus tract

97
Q

• Involves tissues around crown or partially erupted tooth
• Inflammation called pericoronitis
• Flap (lid)of tissue covering tooth is called
operculum
• May have trismus-limited opening
May have elevated temperature

A

Pericoronal

98
Q

• Affects deeper structures as well as gingival margin

Occurs at site of pre-existing periodontitis

A

Periodontal

99
Q
  • Local anesthesia
  • Drain pus
  • Perio instrumentation • Warm saline rinses
  • Schedule follow-up
  • If needed:
  • Adjust pt’s occlusion • Rx antibiotics by DDS
  • Schedule follow-up
A

Gingival/Periodontal

100
Q
  • Local Anesthesia
  • Drain pus
  • Perio instrumentation
  • Irrigate operculum with saline
  • Warm saline rinse
  • Evaluate 3rd molar extraction
  • If needed Rx antibiotics by DDS
A

Pericoronal

101
Q 
• Compromised host immune response (immunosuppressed) 
• HIV 
• Poor oral self-care 
• Emotional stress 
• Increased level of personal stress 
• Inadequate sleep (fatigue) 
• Alcohol abuse 
• Drugabuse 
Smoking 
• Poor nutrition, low protein intake 
• Overall poor nutrition (college students) 
• Pre-existing gingivitis or trauma 
• Avg age is young adult 
	• 22-24 yrs old 
	• But can occur at any age
A

Etiology & Predisposing Factors for NPD

102
Q

• Begins at coronal part of implant
• Implant becomes mobile when it is in final parts of
the disease
• If mobile implant has signs of osseointegration loss,
it is in failure. Shouldn’t be mobile if healthy! • Radiographic signs:
• Vertical destruction of crestal bone around implant
• Bottom portion of implant can still show osseointegration
• May be wedge-shaped defects around implant

A

Peri-Implantitis

103
Q 
Risk Factors for Peri-Implant Failure 
	• Poor biofilm control 
	• Past hx of periodontal disease 
	• Smoking 
	• Residual cement 
Biochemical overload
A

Tx of Failing Implants
• Nonsurgical perio instrumentation • Use of antiseptics
• Local/systemic antibiotics
• Flap surgery

104
Q 
• Plaque-induced 
gingivitis 
	• “Peri-implant gingivitis” 
	• No loss of bone 
	• Reversible if biofilm removed 
	• 80% patients 
50% of implant sites
A

• Peri-implant mucositis

105
Q
  • Periodontitis in soft & hard tissues surrounding osseointegrated implant
  • Progressive bone loss
  • Biofilm-induced inflammation
  • 6-47% prevalence
  • May progress in nonlinear and accelerating pattern
A

• Peri-implantitis

106
Q

• Epithelium adaps to titanium abutment post
Barrier between the implant and the oral
cavity; the soft tissue around an implant
• Sulcular epithelium surrounds the implant abutment post

A

biological seal

107
Q

Osseointegration

A

• Direct contact of bone with implant
surface
• You NEED proper osseointegration for implant to be successful
• Osseointegration successful if: • No mobility
• No inflammation of tissues
• No discomfort during function • No increased bone loss

108
Q
  • Possible to eliminate certain ….factors
  • Faulty restoration
  • Possible to compensate for some that cannot be eliminated easily
  • Improve home care around local crowded teeth
A

Local Contributing Factors

109
Q

• Possible to eliminate …risk factors
• Smoking
IF factors cannot be eliminated, improve the balance by increasing home care or professional care

Such as: 
• Tobacco use
• Diabetes mellitus
• Leukemia
• HIV
• Stress
• Osteoporosis
• Hormonal variations
• Medication side effect
A

Systemic Contributing Factors

110
Q

Patients with well-controlled diabetes have no more periodontal disease than those without diabetes

Patients with poorly-controlled diabetes more likely to develop periodontitis

Patients with diabetes AND smoke 20x more likely to experience severe periodontitis than nondiabetics

A

TRUE

111
Q

• Papilla reacting strongly to the biofilm
• Tumor forms on the interdental gingiva or GM
• Non-cancerous
Not usually painful

A

Pyogenic Granuloma

  • usually in pregant PT
112
Q

Glucose level at appointment time
Target range = 80 to 120 mg/dL
Increased risk of infection = 180–300 g/dL
Unacceptable range = greater than 300 mg/dL

A

Finger-Stick

113
Q

Fungle infection on corners of mouth

A

Cheilosis

114
Q

• If self-care good, usually no problem
• Usually in pts with hx of gingivitis
• Inflammation of gingiva increases even in just small amounts of plaque
Inflammation increases in 2nd & 3rd trimesters due to elevated estrogen create exaggerated response to biofilm

A

Pregnancy
2nd trimester associated with increased Prevotella intermedia levels
• P. intermedia uses estrogen as a substitute for natural growth factor!
• Elevated progesterone increase capillary permeability & dilation àincrease gingival exudate & edema
• Elevated progesterone & estrogen suppress immune response to biofilm

115
Q

Glucose level at appointment time
Target range = 80 to 120 mg/dL
Increased risk of infection = 180–300 g/dL
Unacceptable range = greater than 300 mg/dL

A

Finger-Stick

116
Q

The goal for most individuals with diabetes is a glucose level less than 7%.
High susceptibility to infection occurs when the glucose level is above 8%.

A

HbA1c
HbA1c monitors blood glucose over a period of time
• More accurate in determining monitoring than finger stick

117
Q
  • Increase in hormones result in:

* Increased blood circulation to gingival tissues • Increased sensitivity to local irritants (biofilm)

A

Puberty

• Puberty gingivitis occurs equally in males/females

118
Q
  • Inflammation increases in 2nd & 3rd trimesters due to elevated estrogen create exaggerated response to biofilm
  • 2nd trimester associated with increased Prevotella intermedia levels
  • P. intermedia uses estrogen as a substitute for natural growth factor!
  • Elevated progesterone increase capillary permeability & dilation àincrease gingival exudate & edema
  • Elevated progesterone & estrogen suppress immune response to biofilm
A

Pregnancy
• If self-care good, usually no problem
• Usually in pts with hx of gingivitis
• Inflammation of gingiva increases even in just small amounts of plaque

119
Q
  • Make sure pt’s immune system is okay
  • ANC (absolute neutrophil count) >1000
  • If less than 1000 prophylactic antibiotic needed
  • Platelets = 50,000
  • Viral load or CD4 count does not directly impact dental care
  • Low CD4 count is reflection of advanced disease
  • Chance of opportunistic infections such as candidiasis higher
A

HIV/AIDS & the Dental Hygienist

120
Q
  • Decreased level of hormones result in oral changes
  • Dry mouth/burning sensation
  • Altered taste
  • Bone loss may be exacerbated
  • Menopausal gingivostomatitis
  • Gingiva that bleeds easily
  • Abnormal pale, dry and shiny, erythematous appearance
A

Menopause & the Dental Hygienist
• Talk to pt about osteoporosis risk
• Emphasize self-care to avoid perio problems
• If pt taking bisphosphonates, have pt be aware of oral side effects, especially with IV bisphosphonates

121
Q
  • Most dramatic & clinically obvious
  • Overgrowth usually begins in the papillary area
  • Enlarged papillae can cover the anatomical crown
  • Three major classes of Rx:
  • Anticonvulsants
  • Immunosuppressants
  • Calcium channel blockers
A

Drug-Influenced Gingival Overgrowth

122
Q

Xenograft refers to a graft taken from a human other then the PT receiving the graft

A

FALSE

Xenograft= someone else
Alien

123
Q

Esthetic crown lengthening surgery results in longer clinical crowns for the teeth

A

TRUE

124
Q

When removing sutures following a periosurgical procedure, the suture knot should always be pulled through the tissue

A

FALSE

125
Q

One of the indications for periodontal surgeries to provide acsses for improved perio dontal instrumentation

A

TRUE

126
Q

The term healing by repare means that the architecture and function of lost tissue is completey restored

A

FALSE

127
Q

One relative contraindiction for periodontal surgery can be high risk for dental caries

A

TRUE

128
Q 
• Inflammation of the lungs 
	• Two-types 
• Community-acquired
• Outside hospital setting 
• Hospital-acquired
• During stay in hospital/long term 
	• Perio disease/poor OH may be associated with 
hospital-acquired
A

Pneumonia

129
Q

drugs that help prevent or slow down bone thinning (osteoporosis).

A

Bisphosphonates

130
Q
  • Irregular surface always covered with plaque biofilm
  • Surface harbors bacteria
  • More calculus, more plaque biofilm
  • Difficult/impossible for pt to clean
  • Calculus near perio tissues
A

Calculus
• Supragingival & Subgingival calculus
• 70-90% inorganic (mainly calcium phosphate)
• 10-30% organic (biofilm, dead WBC)

131
Q

1 Attached to pellicle
• Most common on enamel surface
• Removed easily

2 Attached to tooth irregularity
• In cracks in tooth surfaces, grooves on tooth
• Difficult to remove

3 Attached directly to tooth surface
• Interlocked with inorganic crystals of tooth
• Difficult to remove

A

Calculus on Different Surfaces

132
Q
  • Can be surgically removed
  • CEP
  • Flat triangular projection of enamel
  • Spherical shape enamel projection on root
A

Cervical Enamel Projection/Enamel Pearl

133
Q

An important serum marker for CVD and possibly periodontitis
• Produced during acute inflammation
• Successful periodontal therapy could decrease this

A

C-Reactive Protein

134
Q

• NO evidence of CAL or bone loss over 5 years
• Heavy biofilm deposits but low level of tissue
destruction
• Modifiers:
• Nonsmoker
• Normoglycemic patient (non-diabetic)

A

Grade A: Slow Rate

135
Q 
• 2mm or more of CAL over 5 years
• Tissue destruction exceeds expectations based on 
biofilm accumulation 
• Modifiers: 
• Smokers 10+ cigarettes a day
• HbA1c 7% and greater in diabetic pts
A

Grade C: Rapid Rate

136
Q

• Less than 2mm of CAL or bone loss over 5 years
• Tissue destruction meets expectations given biofilm
accumulation in mouth • Modifiers:
• Smokers <10 cigarettes a day
• HbA1c <7% in diabetic patients

A

Grade B: Moderate Rate

137
Q

What stage?
Severity
• Interdental CAL of 1-2mm at site of greatest loss
• Radiographic bone loss extending to coronal 1/3 of root
• No tooth loss due to periodontitis (pt hx)

  • Complexity of Management
  • Max probing depth of 4mm or less
  • Mostly horizontal bone loss
A

Stage I Periodontitis (Mild)

138
Q

what stage?
• Severity
• Interdental CAL of 3-4mm at site of greatest loss
• Radiographic bone loss extending to coronal 1/3 of root
• No tooth loss due to periodontitis (pt hx)

  • Complexity of Management
  • Max probing depth of 5mm or less
  • Mostly horizontal bone loss
A

Stage II Periodontitis (Moderate)

139
Q

What stage?
• Severity
• Interdental CAL greater or equal to 5mm at site of greatest loss
• Radiographic bone loss extends to mid 1/3 of root
• Tooth loss due to periodontitis of 4 or more teeth

  • Complexity of Management
  • Max probing depth of 6mm
  • Vertical bone loss of 3mm or greater
  • Class II or III furcation involvement
  • Moderate alveolar ridge defect complicating implant placement
A

Stage III Periodontitis (Severe)

140
Q

what Stage?
• Severity
• Interdental CAL of greater or equal to 5mm at site of greatest
loss
• Radiographic bone loss extends to mid 1/3 of root
• Tooth loss due to periodontitis of 5 or more teeth
• Complexity of Management
• Max probing depth of greater than 6mm
• Masticatory dysfunction/occlusal trauma
• Tooth mobility > Class II
• Less than 20 remaining teeth

A

Stage IV Periodontitis (Severe)

141
Q
  • Halitosis
  • Dry mouth
  • Staining
  • Perio disease
  • Cancer
A

Oral Problems with Smoking

142
Q

• Affects both the immune & inflammatory system
• Smokers with decreased signs of inflammation due to
impaired blood flow
• Impaired neutrophil function
• May decrease antibody production

A

Impact on Immune System

143
Q

Impact on Bone Metabolism
• Associated with greater bone destruction
• Nicotine may suppress osteoblasts
• May alter normal bone remodeling

A

smoking

144
Q

< 30%

>= 30%

A

localized

generlized

145
Q

Eliminate inflammation in periodontium
• Attempt to restore periodontium back to health
• Combination of professional care & patient’s self-care
• It is the first recommended approach to control perio infections

A

What is NSPT?

Also Known As... 
• Initial perio therapy
• Initial therapy
• Phase I therapy
• Soft tissue management
146
Q

1 Minimize bacterial challenge to patient

2 Eliminate/control local factors for perio disease

3 Minimize impact of systemic factors for perio disease

4 Stabilize the attachment level

A

4 Goals of NSPT

After Professional Tx Has Been Rendered

147
Q
  • Customized OHI
  • Periodontal instrumentation (Scaling/Root Planing)
  • Eliminate local factors
  • Correction of systemic factors
  • Smoking, Diabetes
  • Re-evaluating periodontal response
  • 4-6 week reevaluation after initial NSPT
  • Recare typically in 3 months as perio maintenance
A

Tx Plan Example: Stage I/II, Grade A Periodontitis

148
Q
  • Customized OHI
  • Periodontal instrumentation (Scaling/Root Planing)
  • Eliminate local factors
  • Correction of systemic factors
  • Reevaluation periodontal response
  • 4-6 week reevaluation after initial NSPT
  • Is surgery needed?
A

Tx Plan Example: Stage III/IV, Grade B/C

149
Q
  • Preventive only!
  • Removal of biofilm, calculus, and stains from exposed and unexposed surfaces of the teeth by scaling and polishing as a preventive measure for control of local irritants
A

Oral prophylaxis

150
Q

Removal of calculus, debris, biofilm and byproducts from
tooth surface and gingival pocket to tx inflammation
• This includes scaling, root planing, surgical debridement

A

• Periodontal debridement

151
Q

• There is NO new bone, cementum or PDL formed at the site
• Vulnerable for perio diseases
Probing depth reduction

A

Long Junctional Epithelium

152
Q

• Minimize recurrence & progression of periodontal disease
• Reduce the incidence of tooth loss
• Increase likelihood of detecting & treating other oral
conditions
Expected outcome: maintain the dentition throughout the life of the patient

A

Goals of Periodontal Maintenance

153
Q

1.) Return of disease in patient who has been successfully been tx in the past
• See typical reasons for recurrence in past slide
2.)Disease is resistant to therapy even with appropriate tx and great effort by the patient/clinician

A

Recurrent Periodontitis

154
Q
  • Most are relative contraindications
  • Relative contraindications
  • Conditions that may surgery inadvisable for some when the condition/situations are severe or extreme
  • Patients with:
  • Certain systemic diseases
  • Totally noncompliant with self-care
  • High risk for caries
  • Unreliastic expectations of the outcomes of surgery
A

Perio Surgery Contraindications

155
Q

1 Healing by repair
2 Healing by reattachment
3 Healing by new attachment
4 Healing by regeneration

A

Wound Healing After Surgery

156
Q

• Healing of a wound by formation of tissues that do not precisely restore the original architecture or original function of a body part
• E.g. Formation of a scar after a healing of a cut
• Healing of the peridontium by repair = long junctional
epithelium after perio instrumentation
• This does not duplicate the original perio tissues • NO new bone, cementum or PDL formed

A

Healing by Repair

157
Q

Healing when epithelium & connective tissues are newly attached to tooth root where periodontitis has destroyed this area/attachment

New attachment occurs in area damaged by disease

Reattachment occurs in absence of disease

A

Healing by New Attachment

158
Q

Regrowth of the precise tissues that were present before the disease caused damage to the area

With surgery, regeneration is possible but cannot be regenerated predictably in all sites with current techniques.

A

Healing by Regeneration

159
Q 
1st stage
Occurs when wound margins are closely
adapted
• Ideal situation in perio surgery
but doesn’t happen often
A

Primary Intention

of wound closur

160
Q

Wound margins are not in close contact
• Granulation tissue must form to close the space
• Many in perio surgery involve healing by this

A

Secondary Intention

161
Q

Wound left open with intent of surgically closing later

• Doesn’t pertain to perio surgery

A

Tertiary Intention

162
Q 
To gain access to tooth roots
• Tissue lifted long enough for
whatever procedure
• E.g. Calculus removal
• Afterwards tissue sutured back in
original place
A

Flap for Access

Modified Widman

163
Q 
• Creates a longer clinical crown
• By removing gingival & alveolar bone from necks of
teeth
• Two types:
• Functional crown lengthening
• When there is decay below the GM
• Esthetic crown lengthening
• Improve appearance of teeth related to excess gingiva
A

Crown Lengthening

• Flap elevated for access to bone
• Bone recontoured
• Tissue sutured back in place
• Healing is more apical
position on the root than
before
• Example here: aesthetic
164
Q

Potential for new bone to develop after bone graft

A

Osteogenesis

165
Q

• Grafting materials to form a framework to guide the

formation of new bone within it

A

Osteoconduction

166
Q

Grafting material cells converted into bone-forming cells

to form new bone

A

Osteoinduction

167
Q

Bone from patient’s own body (e.g. exostoses, edentulous ridge)
• Has the most osteogenic potential

A

Autograft

168
Q

Bone taken from another human (e.g. cadaver bone)

A

Allograft

169
Q

• Bone from another species (e.g. bovine)

A

Xenograft

170
Q

• Synthetic material (e.g. calcium phosphate)

A

Alloplast

171
Q 
1.) Does not dissolve in body fluids
• Must be removed by clinician
• Silk
2.) Designed to dissolve over time
• Does not normally need removal
• Some does not dissolve well in
saliva
• Plain & Chromic gut
• Vicryl
A

Nonabsorbable

Absorbable

172
Q

1-Form of oral tablet or capsule/ Antibiotics
2- Placement of chemical agent in perio pocket where it can contact biofilm on
teeth or in the sulcus
• Mouthrinses
• Antibiotic adjuncts

A

Systemic

Topical

173
Q

has properties that make them favorable for use in
periodontitis
• Administered orally (and topically – to be talked about in a bit)
• Higher concentration in GCF
• Effective against A.acetomycetemcomitans
• Inhibit action of collagenase
• Enzyme responsible for breakdown of periodontium

A

Tetracycline

174
Q

Doxycycline Hyclate Gel

A 
Atridox=Brand name
• Brand name: Atridox
• Tetracycline derivative
• Gel into the periodontal pocket
• Two syringes: liquid & powder
• Mix together into one syringe
• Injected into the pocket
• Gel solidifies when in contact with GCF
• Adjunct to SRP for local periodontitis
• Same Adverse Rxns and Contraindications as Minocycline
175
Q

• Brand name: PerioChip
• Gelatin chip containing 2.5mg of CHX
• Inserted into pocket
• May be used in pockets 5mm or greater
• Upto 8 chips can be inserted in 1 visit
• Depending on the size it may need to be cut into
size
• Chip dissolves in the pocket over 7-10 days
• Can be replaced at 3 month recare visit
• No risk of antibiotic resistance since it’s not an
antibiotic

A

Chlorhexidine

Gluconate Chip

176
Q 
Minocycline hydrochloride microspheres
• Arestin
• Doxycycline hyclate gel
• Atridox
• Chlorhexidine gluconate chip
• Periochip
A

Examples of Controlled-Released Agents

177
Q 
• Brand name: Arestin
• Powder microsphere form
• Broad-spectrum
• Tetracycline derivative
• Microspheres dissolve after 5-7 days
• Adjunct to SRP in patients with
localized periodontitis
A

Minocycline Hydrochloride Microsphere

178
Q

Only by Rx (Peridex, Paroex, Perioguard)
• 0.12% concentration only in the United States
• Proven to reduce gingivitis
• Reduce severity of gingivitis by about 50% with
proper use
• Bactericidal agent against gram + and – bacteria
• Disrupts cell walls of bacteria
• Has low level of toxicity
• Has good substantivity
• Binds to hard & soft oral tissues

A

Chlorhexidine Gluconate

179
Q
  • Mouth irritation
  • Extrinsic tooth staining
  • Brown
  • Xerostomia
  • Taste changes
  • Unpleasant or unusual taste
  • Metallic taste
  • Increases SUPRAGINGIVAL calculus formation
A

Chlorhexidine Gluconate: Side Effects

180
Q 
Common active ingredient in many mouthrinses
• Essential oils include:
• Thymol
• Menthol
• Eucalyptol
• Methylsalicylate
• Available OTC
• Some have ADA seal for use against gingivitis
• Can help control biofilm
• Less expensive than CHX
A

Mouthrinses with Essential Oils

Side Effects
• Burning sensation
• Bitter taste
• Drying of mucous membrane

summer (3 decks)

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