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Board Review > Periodontology > Flashcards

Periodontology Flashcards

1
Q

What are the tissues of the Peridontium?

A

PDL, Gingiva, Cementum, and Alveolar bone.

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2
Q

What are the functions of the PDL?

A

Made of fiber bundles and cells.
Tooth anchorage, transmits occlusal forces to the bone and resists impact of these forces, supplies nutrients to periodontal structures, sensory functions include touch, pressure and pain, shock absorber for the teeth, nerves and blood vessels.

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3
Q

Where do the PDL fibers attach to?

A

Tooth’s cementum

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4
Q

Sharpey’s fibers

A

Fiber bundles that are attached ad embedded in cementum and bone.

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5
Q

Transseptal Fibers

A

“interdental ligament”, interproximally, hold teeth in interproximal contact with each other. Horizontal

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6
Q

Alveolar crest fibers

A

Located apical to the junctional epithelium. Resists tilting and horizontal forces.

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7
Q

Oblique fibers

A

Most numerous type of fiber, resists “intrusive” or “vertical” masticatory forces. Prevents the tooth from being “jammed” into the bony socket. Diagonal

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8
Q

Horizontal fibers

A

resist horizontal and tilting forces. Horizontal running.

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9
Q

Apical Fibers

A

Prevents the tooth from being lifted out of the bony socket. Resists “extrusive forces”. Extend from apical area of tooth to base of tooth socket.

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10
Q

Interradicular fibers

A

Found only in multi-rooted teeth, located in tooth furcations, and stabilizes tooth root.

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11
Q

Most common cell of PDL, important in collagen synthesis, and fiber production. “Primary cell of the PDL”

A

Fibroblasts

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12
Q

Production of bone

A

Osteoblasts

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13
Q

Resorption (break down) of bone

A

Osteoclasts

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14
Q

Production of cementum

A

Cementoblasts

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15
Q

Resorption of cementum

A

Cementoclasts

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16
Q

Signs of a healthy gingiva

A

Firm, light pink, fills interproximal spaces, knife-edged, gingival margin on enamel, 1-3 mm gingival sulcus

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17
Q

Signs of unhealthy gingiva

A

Spongy, swollen, red, bleeds upon probing, bulbous, festooned, recession, hyperplastic, deep pockets or probing depths.

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18
Q

Reversible inflammation of the gingiva, directly related to plaque accumulation, results from ulceration at the base of the sulcus.

A

Gingivitis

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19
Q

What is most gingivitis termed?

A

Chronic plaque-associated gingivitis

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20
Q

Signs of acute gingivitis?

A

Develops rapidly, obvious inflammation, may be painful, neutrophil is the most prevalent cell.

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21
Q

Signs of chronic gingivitis

A

Develops slowly, may appear normal, not usually painful.

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22
Q

Where is cyanosis of the gingiva often found?

A

Bluish, highly vascular and often found around crowns

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23
Q

What is pallor gingiva associated with?

A

Lighter than normal, associated with anemia, leukemia, and fibrotic tissue.

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24
Q

This gingiva is stippled and this one is not.

A

Attached gingiva is stippled and marginal gingiva is not

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25
Q

What is edematous?

A

Glossy appearance due to increased fluid. Edema is the result of vasodilation of the peripheral circulation

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26
Q

Increase in cellular and fibrous components, may present with pallor.

A

Fibrotic

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27
Q

How is stillmans cleft indicated?

A

By vertical loss of tissue, caused by improper flossing, bulbous, and blunted

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28
Q

Inner tube-like swelling at gingival margin, due to inflammation and an increased cell number.

A

Festoon

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29
Q

Caused by age, plaque, iatrogenic, tooth malposition, Occlusion, Frenum pull, trauma, inadequate attachment, improper flossing technique.

A

Recession

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30
Q

Drugs that increase the risk of gingival enlargement

A

Phenytoin (Dilantin)
Nifedipine (procardia)
Cyclosporin

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31
Q

Other causes of gingival enlargement.

A

Mouthbreathing, periodontal inflammation, genetic/hereditary factors, systemic conditions like leukemia and hormonal imbalance.

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32
Q

Gingival enlargement due to an increase in cell numbers.

A

Hyperplasia

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33
Q

Gingival enlargement fit to an increase in cell size

A

Hypertrophy

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34
Q

Oval-shaped root exposure apical to the CEJ, alveolar bone loss and root exposure.

A

Dehiscence

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35
Q

Window-like opening in the bone covering the roof of a tooth and bordered by alveolar bone on the coronal aspect of the tooth.

A

Fenestration

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36
Q

Major etiology factor in the initiation and progression of inflammatory periodontal diseases, known as biofilm which is bacteria forming on tooth surfaces.

A

Dental Plaque

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37
Q

How is Plaque formed?

A

Glycoproteins from saliva are absorbed to the tooth surface, forming the acquired pellicle.
Bacteria then adhere to the acquired pellicle
Bacteria multiply to form colonies on the tooth, creating a biofilm
As Plaque grows, bacteria detach from the biofilm and become “planktonic” bacteria (free)
Later, calculus forms from the mineralized Plaque biofilm

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38
Q

Cocci

A

Round/spherical-shaped bacteria found in early Plaque formation.

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39
Q

Bacilli

A

Rod-shaped bacteria, most common type found in periodontal disease.

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40
Q

Spirochetes

A

Spiral-shaped bacteria, often associated with NUG/NUP.

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41
Q

Aerobic

A

Require oxygen to grow, NOT found in periodontal pockets

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42
Q

Anaerobic

A

Grow in the absence of oxygen, found in periodontal pockets and gingival sulcus.

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43
Q

Faculative anaerobic

A

Can grow in presence of oxygen or absence of oxygen.

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44
Q

Streptococcus: s. Mitis, s. Oralis, s. Sanguis, and s. Mutans are all gram positive bacteria.

A

Early “healthy” Plaque, able to attach to the acquired pellicle.

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45
Q

Actinomyces: a. Viscous is an example of a gram positive rod and?

A

Early colonizer in Plaque formation

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46
Q

Most common/most important periodontal pathogen, is an anaerobic gram negative rod shaped bacteria.

A

Porphyromonas Gingivalis (P. Gingivalis)

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47
Q

This is a spirochete

A

Treponema denticola (t. Denticola)

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48
Q

Pathogen in adult periodontitis

A

Tannerella forsythia

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49
Q

Plays a critical role in biofilm formation, anaerobic gram negative rod shaped bacteria

A

Fusobacterium nucleatum

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50
Q

Associated with periodontal disease, gram negative facultative anaerobes associated with inflammation during pregnancy

A

Campylobacter rectus ( C. Rectus)

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51
Q

Associated with periodontal disease, gram negative anaerobe most often associated with inflammation during pregnancy

A

Prevotella intermedia

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52
Q

Gram negative rod-shaped bacteria associated with aggressive periodontal disease

A

Aggregatibacter actinomycetemcomitans

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53
Q

Bacterial species associated with NUG/NUP

A

T. Denticola, P. Intermedia, P. Gingivalis, and fusobacterium

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54
Q

What are the Plaque-retentive zones?

A

Pits and fissures, irregular tooth surfaces and interproximal areas

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55
Q

What makes up the bulk of the Plaque biofilm and functions to hold the bacteria together, allow for exchange of nutrients and removal of waste products.

A

Extra cellular matrix

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56
Q

Pellicle formation is derived from salivary glycoproteins
Sticky matrix that allows for bacterial attachment to the tooth
Attachment begins with gram positive cocci
As Plaque matures, more facultative anaerobic bacteria are present.

A

Supragingival

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57
Q

Accumulates after supragingival Plaque
More motile bacteria, gram negative anaerobic than supragingival Plaque
Free-floating or loosely adherent Plaque in the pocket/sulcus

A

Subgingival

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58
Q

Densely interconnected
Contains non-motile bacteria
May mineralize and become calculus

A

Adherent

59
Q

Also known as planktonic Plaque
Mostly motile rods and spirochetes
Increase during acute infection/inflammation

A

Non-adherent

60
Q

What oral hygiene aid is most suited for removal of loose or non-adherent Plaque?

A

Oral irrigator

61
Q

What do poorly fitted crowns cause?

A

Marginal inflammation, overhangs, food impaction, often caused by open contacts between teeth.

62
Q

What often contributes to tissue destruction?

A

Bacterial products such as endotoxins, collagenase, protease, hyaluronidase, and exotoxins.

63
Q

Associated with gram negative bacteria, stimulate osteoclasts, and inhibits fibroblasts and May harm neutrophils (PMNs)

A

Endotoxins

64
Q

Directly breaks down connective tissues

A

Collagenase

65
Q

Directly breaks down tissues

A

Protease

66
Q

Breaks down the extra cellular matrix, allowing bacteria to detach “spreading factor”.

A

Hyaluronidase

67
Q

Bacterial waste products that cause direct tissue injury, examples: hydrogen sulfite, uric acid and fatty acids

A

Exotoxins

68
Q

Inflammation of the periodontal tissues, and loss of CT attachment to the tooth, characterized by the apical (downward) migration of the JE, the rat of destruction varies due to the virulence of bacteria and the host response.

A

Periodontitis

69
Q

How is periodontitis documented?

A

By CAL over time

70
Q

Measures from the CEJ to the base of the pocket, best indicator of damage to the periodontium, means disease progression.

A

CAL

71
Q

How is CAL measured?

A

Measure the pocket depth first
Measure how much recession is present
Add two numbers together

72
Q

What is the best instrument to detect a Furcation?

A

Nabers probe

73
Q

What is the attached gingiva connected to?

A

Tooth cementum and the periosteum of the alveolar bone

74
Q

What is NOT calculated for palatial surfaces?

A

Width of attached gingiva

75
Q

Signs of healthy periodontium.

A

Intact, distinct RO lamina dura should be present.
PDL space should be visible and uniform width.
Crest of alveolar bone should be 1-2 mm apical to the CEJ.

76
Q

Signs of disease/periodontitis

A

Loss of bone in Furcation areas
Bone loss vertical or horizontal
Best evaluated on bitewing radiographs
Lamina dura becomes less distinct

77
Q

Tooth mobility

A

Class 1: slight, up to 1 mm horizontally (facial-lingual)
Class 2: moderate, 1-2 mm horizontal (facial-lingual)
Class 3: severe, >2 mm horizontal/vertical (depressable in the socket)

78
Q

How do you check for mobility?

A

Two instruments with hard handles

79
Q

Occur ABOVE (coronal to) the alveolar crest of bone.

A

Suprabony pockets

80
Q

Base of pocket is BELOW (apical to) the alveolar crest and treated with regenerative procedures.

A

Infrabony pockets

81
Q

What does increased pocket/probing depth occur from?

A

Coronal movement of the gingival margin, “pseudopockets” due to inflammation and swelling, deepening of the sulcus/pocket due to loss of attachment to tooth, apical margination of the JE

82
Q

This DOES NOT cause periodontal disease.

A

Occlusal Trauma

83
Q

Excessive force on a tooth with normal bone support

A

Primary occlusal trauma

84
Q

Result of forces applied to a tooth that has previously experienced bone or attachment loss.

A

Secondary occlusal trauma

85
Q

What may result from excessive occlusal forces on a tooth that has bone/attachment loss previously?

A

Rapid bone loss/pocket formation

86
Q

Signs/symptoms of occlusal trauma.

A 
Sensitivity
Wear facets
Tooth migration
Increased mobility
Widening of PDL space on radiograph
87
Q

Associated with dental Plaque (bacteria) only, but may be modified by systemic factors, nutrition and meds

A

Plaque-induced gingival disease

88
Q

Associated with viruses, fungus, genetic or systemic conditions. May also result from trauma or foreign body reactions. Gingival inflammation may be caused by open contacts and subgingival margins of restorations.

A

Non-Plaque induced gingival disease

89
Q

Examples of non-Plaque induced gingival disease.

A 
Primary Herpes 
Recurrent herpes (cold sores, fever blisters)
Aphthous ulcers (canker sores)
90
Q

What is chronic periodontitis classified as?

A

Localized or generalized

91
Q

What is aggressive periodontitis classified as and associated with?

A

Localized or generalized and associated with aggregatibacter actinomycetemcomitans(Aa)

92
Q

Periodontitis as a manifestation of systemic diseases

A

Examples include acquired neutropenia and leukemia

93
Q

A lack deficiency of neutrophils (polymorphonuclear leukocytes)

A

Neutropenia

94
Q

Periodontitis associated with genetic disorders

A 
Familial and cyclic neutropenia 
Down syndrome (but no increased risk for caries)
Papillon-LaFevre syndrome (severe periodontal destruction, premature tooth loss, hyperkeratosis of palms of hands and soles of feet)
Chediak-Higashi syndrome (inherited dx of of immune and nervous systems, impairment of neutrophils, and aggressive periodontitis associated with this)
95
Q

Necrotizing Ulcerative Periodontitis

A

Loss of clinical attachment and bone

96
Q

Necrotizing ulcerative gingivitis

A

Affects gingiva only

97
Q

(treponema denticola), prevotella intermedia, porphyromonas Gingivalis And fusobacterium

A

Remember-associated with spirochetes

98
Q

What’s the drug of choice for necrotizing periodontal diseases?

A

Tetracycline, because it concentrates in gingival crevicular fluid

99
Q

What are the clinical findings of necrotizing periodontal diseases?

A

“Punched out” papillae, pseudomembrane, fetid bad odor, pain and severe inflammation

100
Q

Results from injury to or infection of the surface gingival tissue.

A

Gingival Abscess

101
Q

Results when infection spreads deep into pocket, and drainage is blocked, may develop after periodontal debridement.

A

Periodontal abscess

102
Q

Develops in inflamed dental follicular tissue, overlying the crown of a partially erupted tooth (most often mandibular third molars), often does NOT show up on a radiograph.

A

Pericoronal abscess

103
Q

Infection of the tooth pulp, secondary to deep dental caries, diagnosis often requires a periapical radiograph.

A

Periapical Abscess

104
Q

Localized tooth-related factors that may increase the risk of developing Plaque-induced gingivitis and periodontitis, or exacerbate these conditions:

A

Gingival recession, lack of attached gingiva, frenum position and “pull”, enlarged/excessive gingiva, and occlusal trauma.

105
Q

2-4 days, no clinical changes, vasodilation of small capillaries, increased flow of gingival fluid.

A

Stage I, Initial lesion

106
Q

4-7 days, clinical signs of gingivitis appear, collagen destruction, bleeding occurs due to ulcerated sulcular lining, PMNs found in sulcus.

A

Stage II, Early lesion or gingivitis

107
Q

2-3 weeks, capillary proliferation (overgrowth) causes erythema, gingival enlargement may increase probing depths

A

Stage III, established lesion

108
Q

3 weeks + to years, transition from gingivitis to periodontitis, irreversible, JE detaches from root surface and migrates apically, osteoclasts And bone loss.

A

Stage IV, Advanced lesion

109
Q

Events occurring as periodontal disease progresses?

A

Increased probing depths, increased attachment loss and increased bone resorption

110
Q

Transient (temporary) vasoconstriction first,

A

Then vasodilation

111
Q

Excess of blood in the vessels in the tissues

A

Hyperemia

112
Q

Movement of WBCs to the periphery of vessel walls

A

Margination

113
Q

WBCs line the wall of the vessel

A

Pavementing

114
Q

Process by which neutrophils squeeze between endothelial cells in the vessel wall

A

Diapidesis

115
Q

Cells move into the tissues from the blood vessel

A

Emigration

116
Q

Movement of cells to the site of inflammation

A

Chemotaxis

117
Q

Significant to development and progression of disease, most prevalent in acute inflammation, may active in the periodontal pocket, and main function is phagocytosis

A

Neutrophils

118
Q

Increased risk of periodontal disease, xerostomia and increased caries risk, candidiasis, and delayed wound healing

A

Diabetes mellitus

119
Q

Vitamin C deficiency, it is necessary for collagen production and wound healing

A

Scurvy

120
Q

Protein deficiency, proteins are necessary for a healthy periodontium

A

Kwashiorkor

121
Q

Erythroblastic anemia, cyclic neutropenia, radiation therapy and acute mono grid leukemia can all affect periodontal tissues

A

Blood cell dyscrasias

122
Q

Prevotella intermedia and campylobacter rectus, meds, puberty, menstruation, and menopause can all affect periodontal tissues

A

Hormonal effects: pregnancy gingivitis

123
Q

Are at an increased risk of developing periodontal disease due to vasoconstriction, NOT at an increased risk of developing caries, have deeper pockets and more bone loss, may develop “black hairy tongue”.

A

Smokers

124
Q

Cancer patients may present with?

A

Xerostomia, mucositis, dysgeusia (loss of taste or altered taste), increased risk of fungal and viral infections.

125
Q

Patients who are HIV + may present with?

A

Linear gingival erythema (band of redness of the marginal gingiva), NUP (necrosis of gingiva and alveolar bone), Aphthous ulcers, Kaposi’s sarcoma (malignancy of vessels, presents as a blue/purple macule)

126
Q

Objectives of periodontal therapy?

A

Identify the disease, control inflammation and deal with defects resulting from the disease.

127
Q

Goals of periodontal surgery?

A

Allow easier cleaning for the patient, replace lost tissue, and gain new attachment

128
Q

What happens after periodontal therapy?

A

Re-evaluation appointment 4-6 weeks after therapy is necessary to determine effectiveness and the first factor to assess at this appointment is the degree of inflammation of the tissues.

129
Q

Factors that affect the prognosis after treatment?

A

Tooth mobility, endosperm tic status, depth and width of pockets, the more bony walls present the better the prognosis, a 3 wall defect has a better prognosis than all wall defect.

130
Q

Treatment of periodontal disease?

A

SRP, antimicrobials/antibiotics, gingivectomy, Osseous surgery, periodontal dressings, and regenerative procedures.

131
Q

Most common surgical procedure to reduce pocket depths, removes soft tissue only, and treatment for gingival hyperplasia and pseudopockets.

A

Gingivectomy

132
Q

Requires gingival flap (incision), bone recontoured (osteoplasty), bone removed (osteoectomy), sutures are required.

A

Osseous surgery

133
Q

Rarely used, used for protection, comfort and to maintain tissue contour. “White patches” can occur after dressing is removed which are composed of dead cells and tissue debris, and DO NOT prevent Plaque build up.

A

Periodontal Dressings

134
Q

Uses barrier membrane to block migration of epithelial cells, Osseous and soft tissue grafts are examples of regenerative procedures, main reason is to treat infrabony defects.

A

Guided Tissue Regeneration

135
Q

What does tissue repair generally involve?

A

Fibrous repair through the formation of granulation tissue.

136
Q

Initial tissue formed in the CT after injury, is an immature tissue with many capillaries (neovascularization) and fibroblasts.

A

Granulation tissue

137
Q

What are the four stages of fibrous repair?

A

Blood clotting, wound cleansing, tissue rebuilding and wound remodeling.

138
Q

Is composed of fibrin, fibronectin, and platelets. It fills the wound serving as a scaffolding for PMNs and macrophages.

A

Blood clotting

139
Q

Macrophages invest debris and degrade the clot, PMNs attack bacteria, new capillaries and fibroblasts move in debris is removed.

A

Wound cleansing

140
Q

Fibroblasts synthesize/deposit fibronectin, collagen and proteoglycans. Granulation tissue is formed, and is highly cellular and vascular.

A

Tissue rebuilding

141
Q

Granulation tissue is eventually remodeled into a scar composed of dense collagen interspersed with cells and blood vessels.

A

Wound remodeling

142
Q

When is arachidonic acid produced and why is it metabolized?

A

Produced when there is a tissue injury and metabolized to produced inflammatory mediators.

143
Q

Cause swelling, pain and inflammation. Inhibited by NSAIDs and aspirin.

A

Prostaglandins

144
Q

Cause bronchoconstriction, cellular infiltration, cytokines release and inflammation. Derived from leukocytes especially mast cells and inhibited by asthma drugs such as singular.

A

Leukotrienes

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