Oral Exam Studyguide Flashcards by Annabella Moody

Primary factors:

Plaque AND a susceptible host

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Contributing factors (systemic):

DM
HIV/AIDS
Smoking

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What is a clinical sign a periodontist may see clinically?

Multiple periodontal abscesses due to P. Gingivalis

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What may be a clinical sign of a patient who smokes?

Diminished BOP (caused by vasoconstriction)

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Local contributing factors:

trauma from occlusion
root proximity
overhangs
calculus
smoking
socioeconomic factors

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Primary periodontal pathogens:

Streptococcus species
Hemophilus species
Neisseria species
Actinomyces species
Veillonella species

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Mechanism of primary periodontal pathogens:

adhesion to pellicle

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Mechanism of secondary colonizers:

co-adhesion to primary colonizers

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Secondary periodontal pathogens:

Prevotella intermedia
Capnocytophaga species
Fusobacterium nucleatum
Porphyromonas gingivalis

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Red complex bacteria:

P. gingivalis
B. Forsythia
T. Denticola

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Pathogen responsible for localized aggressive periodontitis:

Aggregataibacter actinomyceteconcomitans

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What is plaque:

A structural and functional organized, species-rich microbial biofilm formed on teeth

70% water + 30% microorganisms + intracellular matrix

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What is calculus:

Mineralized plaque

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What is materia alba:

Non-organized, soft accumulation of salivary proteins, bacteria, epithelial cells, and food debris

Easily displacable with air/water spray

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Bacteria most-associated with periodontal abscess in diabetic patients:

Porphyromas gingivalis

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Bacteria associated with pregnancy induced perio problems:

Prevotella intermedia

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Pathogens associated with health vs. disease:

Health: gram postitive, cocci, non-motile, facultative anaerobes and fermenting

Disease: gram negative, rod, motile, obligate anaerobes and proteolytic

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What is the difference between supragingival and subgingival calculus:

Supragingival calculus: derives minerals from saliva; gram positive, cocci & rods (aerobic)

Subgingival calculus: derives minerals from inflammatory exudate and GCF; more mineralized; gram negative, rods and spirochetes (anaerobic)

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Mucocutaneous diseases affecting the periodontium:

desquamative gingivitis (clinical term not a diagnosis)
Lichen planus
mucous membrane pemphigoid
pemphigus vulgaris
lupus erythematosus
erythema multiforme
necrotizing stomatitis

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Periodontal manifestations with pregnancy:

Gingivitis, many microbes thrive with increased progesterone

Primary bacteria: Prevotella intermedia

Increased inflammatory response, gingival enlargement, pseudopockets

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Periodontal manifestations with diabetes:

Decreased salivary flow
elevated salivary & GCF glucose levels
elevated gram-negative bacteria and candida albicans

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Periodontal manifestations of leukemia:

oral ulcerations
gingival bleeding
recurrent infections
existing perio can be exavcerbated

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Oral manifestations of HIV/AIDS:

candidiasis
viral lesions
major apthous uclers
necrotizing gingivitis
linear gingival erythema
necrotizing periodontitis
neoplasms
oral hairyy leukoplakia
Kaposi sarcoma
Non-hodgekins lymphoma

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HIV-induced gingivitis:

Characterized by linear gingival erythema (seen in 15-30% of patients)

Most severe form is necrotizing stomatitis

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HIV-induced periodontitis:

Seen in 0-5% of patients and is usually localized

Periodontal manifestations of transplant patients:

Common immunosuppressive drug is cyclosporine --> causes 30% incidence of gingival overgrowth

Periodontal manifestations of epilepsy:

Common anti-seizure drug is Dilantin (phenytoin) and that causes a 50% incidence of gingival overgrowth

Immunologic effects for periodontal disease? How?

Patient not able to fight off bacteria

Pathogenesis of perio disease: Predominant cells of EARLY lesion:

Early lesion = 4-7 days --> T cells

Pathogenesis of perio disease: Predominant cells of ESTABLISHED lesion:

Established lesion = 14-21 days --> B cells/Plasma cells

Does age make a difference in the progression/severity of perio disease?

Yes; better prognosis if older because % bone loss / age

How are periodontal tissues destroyed in periodontal disease?

1. bacterial invasion 2. immune response (cytokines, inflammatory mediators) 3. enzyme release (collagenase, protease) 4. bone and tissue destruction 1. increased plaque 2. increased inflammation 3. HIGH GCF flow 4. gram neg facultative anaerobes (which produce tissue destructive virulence factors such as LPS, leukotoxin, gingipains, collagenase, protease)

What does BOP mean?

Microulcerations of sulcular epithelium

What is the EARLIEST sign of gingival inflammation?

BOP

What is a situation in which we may see decreased BOP?

Smoking; vasoconstriction (suppressed immune response)

A normal, healthy patient:

ASA 1

A patient with mild systemic disease: (ex. pregnancy)\, controlled HTN, etc.)

ASA 2

A patient with severe systemic disease: (ex. a hx of MI more than 3 mo ago, poorly controlled diabetic, etc.)

ASA 3

A patient with severe systemic disease that is a constant threat to life: (ex. a recent MI within less than 3 mo)

ASA 4

A moribund patient that is not expected to survive without operation:

ASA 5

A declared brain-dead patient whose organs are being removed for donor purposes:

ASA 6

Gingivitis is ____ induced:

Plaque

What are the clinical signs of gingivitis?

1. inflammation- BOP and edema 2. NO destruction of PDL and bone 3. NO apical migration of JE 4. Reversible

1. Plaque induced: _____ 2. Inflammation- edema and BOP:_____ 3. No destruction of PDL and bone:___ 4. Destruction of PDL and bone:____ 5. No apical migration of JE: ____ 6. Apical migration of JE: _____ 7. Reversible: _____ 8. Irreversible but can be brought to state of stability on reduced periodontium: ______

1. both 2. both 3. gingivitis 4. periodontitis 5. gingivitis 6. periodontitis 7. gingivitis 8. periodontitis

What determines if gingivitis progresses to periodontitis?

Susceptible host

Traumatic occlusal forces applied to a tooth or teeth with NORMAL periodontal support. -clinically you may see ADAPTIVE MOBILITY -ex: high restoration with mobility that will resolve when the restoration is fixed

Primary occlusal trauma

Injury resulting in tissue changes from normal or traumatic occlusal forces applied to a tooth or teeth with REDUCED periodontal support. -clinically: progressive mobility

Secondary occlusal trauma

Orthodontic forces can adversely effect the periodontium and cause root resportion, pulpal disorders, gingival recession, and alveolar bone loss

Orthodontic induced occlusal trauma

What components of the periodontium can be affected by trauma from occlusion? What is NOT affected?

Affected: cementum, PDL, alveolar bone proper NOT affected: gingiva, JE

T/F: Trauma from occlusion in the absence of inflammation DOES NOT cause pocket formation to lead to loss of connective tissue

TRUE

Clinical signs of trauma from occlusion:

1. mobility 2. thickened PDL 3. Hx of bruxism 4. missing or tilted teeth 5. evidence of occlusal interferences

Palpable or visible movement of tooth when subject to occlusal forces:

Fremitus

How should you determine mobility of tooth?

Using two ends of rigid instruments NOT fingers

What classification is used to determine mobility?

Millers classification

Normal physiologic movement when force is applied to tooth:

Millers Class 0

Mobility greater than physiologic, first distinguishable sign of movement:

Miller Class 1

Tooth can be moved up to 1mm from its normal position in a lateral direction (BL or MD):

Miller Class 2

Tooth can be moved 1mm or more in a lateral direction (BL or MD), and able to depress tooth:

Miller Class 3

Furcation classification are based on:

Glickman/Goldman

-Pocket formation into flute of furca -Inter-radicular bone intact

Glickman Grade 1 Goldman incipient

-Pocket formation of varying depths into the furca but NOT completely through to the other side -Loss of inter-radicular bone -Can be shallow or deep

Glickman Grade 2 Goldman Cul-de-sac

-Pocket formation allowing probe to pass completely through to other side -Complete loss of inter-radicular bone

Glickman Grade 3 Goldman through and through

-Loss of attachment and gingival recession that has made the furcation clearly visible to clinical examination

Glickman Grade 4

Grade/Class II or III furcation involement automatically places patient in ____ stage of perio

III or IV

-Gingival recession with NO loss of interproximal attachment -CEJ not detected M or D

RT 1

-Gingival recession WITH loss of interproximal attachment -Interproximal attachment loss is less than or equal to buccal attachment loss

RT 2

-Gingival recession WITH loss of interproximal attachment -Interproximal attachment loss is greater than buccal attachment loss

RT 3

Loss of interproximal attachment leads to decreased blood supply which results in a poor prognosis after treatment or grafting: -RT 1: -RT 2: -RT 3:

RT 1: 100% root coverage detected RT 2: Mixed results RT 3: Full coverage NOT achievable

54.5% of young adults have a:

mucogingival defect (gingival recession)

What type of defect is most common?

2-wall defect

What type of defect has the best prognosis?

3-wall defect

Vertical bone loss is classified based on:

The number of walls remaining

Horizontal bone loss is equal on all surfaces because:

There are no walls and results in flat interproximal bone

4 main components of periodontium:

1. gingiva 2. cementum 3. PDL 4. Alveolar bone proper