Perio Final Flashcards

1
Q

Most common chromosomal anomaly in humans, affecting about 5,000 babies born each year and more than 350,000 people in the United States

A

Trisomy 21

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2
Q

Genetic condition caused by an extra chromosome of the 21st chromosome (47 instead of 46)

A

Trisomy 21

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3
Q

Generalized early periodontitis, begins in the deciduous dentition and continues in the adult dentition

A

Trisomy 21

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4
Q

Prevalence and severity of perio is extremely high when compared to either their siblings or other mentally challenged individuals

A

Trisomy 21

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5
Q

Where are the most frequent sites of perio destruction in pts with Trisomy 21?

A

Molars
Incisors

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6
Q

The roots of the lower incisors are characteristically short which, in combination with the loss of bone, predisposes to premature tooth loss

A

Trisomy 21

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7
Q

Delayed eruption of both primary/permanent dentitions, microdontia, macroglossia

A

Trisomy 21

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8
Q

Molecular biology research has underlined the
important role of several cell-cell adhesion
receptors on the neutrophil surface; emphasizing
that defects in numbers of these receptors may
lead to increased susceptibility to infectious
disease

A

Leukocyte-adhesin deficiency syndrome

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9
Q

Associated w/ perio, oral ulcers, and chronic necrotic skin lesions

A

Leukocyte-adhesin deficiency syndrome

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10
Q

An inborn error of metabolism with highly variable clinical severity caused by loss-of-function mutations in the gene encoding tissue nonspecific alkaline phosphatase (TNSALP)

A

Hypophosphatasia (HPP)

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11
Q

Decreased serum alkaline phosphatase and severe loss of alveolar bone and premature loss of the deciduous teeth, particularly in the anterior region

A

Hypophosphatasia (HPP)

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12
Q

Mutated Gene CTSC

A

Papillon-Lefevre syndrome

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13
Q

Encodes for cathepsin C, key activator of serine proteases in immune cells

A

Papillon-Lefevre syndrome

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14
Q

Autosomal recessive, characterized by the presence of hyperkeratotic skin lesions

A

Papillon-Lefevre syndrome

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15
Q

Exhibits diffuse palmar and plantar keratosis

A

Papillon-Lefevre syndrome

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16
Q

Severe generalized periodontitis, commonly before puberty with early loss of deciduous and permanent teeth

A

Papillon-Lefevre syndrome

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17
Q

Teeth are lost in order of eruption and as yet there is no general agreement on the success of dental therapy

A

Papillon-Lefevre syndrome

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18
Q

Associated with complete edentulism early in life

A

Papillon-Lefevre syndrome

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19
Q

Chemotaxis association

A

Papillon-Lefevre syndrome

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20
Q

LYST gene lysosomal trafficking regulator protein affecting phagocytosis

A

Chediak-Higashi syndrome

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21
Q

Autosomal recessive trait associated with severe periodontitis

A

Chediak-Higashi syndrome

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22
Q

Neutrophil chemotaxis and bactericidal functions are abnormal in these patients

A

Chediak-Higashi syndrome

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23
Q

Immune system abnormalities, bleeding abnormalities, and multiple infections

A

Chediak-Higashi syndrome

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24
Q

C1R and C1S serine proteases of the complement cascade

A

Ehrlers-Danlos syndrome

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25
Q

Inherited CT disorders exhibiting joint
hypermobility (joints that stretch further than normal), skin hyperextensibility (skin that can be
stretched further than normal), and tissue fragility

A

Ehrlers-Danlos syndrome

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26
Q

Autosomal dominant and reclassified into 13 sub-types on the basis of inheritance and clinical presentation

A

Ehrlers-Danlos syndrome

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27
Q

Which types of Ehrlers-Danlos syndrome have increased susceptibility to periodontitis?

A

IV and VIII

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28
Q

Which type of Ehrlers-Danlos syndrome is associated with fragile oral mucosa and blood vessels?

A

VIII

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29
Q

Severe generalized periodontitis with an early onset

A

Ehrlers-Danlos syndrome

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30
Q

Children exhibit severe inflammation of
gingiva and complications include arterial or GI ruptures

A

Ehrlers-Danlos syndrome

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31
Q

Clinical term not a diagnosis; lab procedures necessitate a full diagnosis

A

Desquamative gingivitis

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32
Q

Nikolsky sign

A

Desquamative gingivitis

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33
Q

Blister formation when pressure is applied to the skin or mucosa with vesiculobullous disorders

A

Desquamative gingivitis

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34
Q

Systemic inflammatory autoimmune disease production of anti-citrullinated protein antibodies leading to synovial joint inflammation and destruction

A

Rheumatoid arthritis

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35
Q

Number of missing teeth is 4x greater in pts with this disease

A

Rheumatoid arthritis

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36
Q

Increased bleeding, gingivitis and increased probing depths in pts with this disease

A

Rheumatoid arthritis

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37
Q

Prevalence of this disease in PD patients is higher compared to periodontally matched healthy controls

A

Rheumatoid arthritis

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38
Q

P gingivalis expresses PPAD enzyme leading to ________ production

A

ACPA

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39
Q

A. actinomycetmecomitans leads to hypercitrullination of what cells?

A

Neutrophils

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40
Q

DNA of bacteria such as P. gingivalis detected in the synovial fluid of pts with what disease?

A

Rheumatoid arthritis

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41
Q

What induces the formation of pro-inflammatory cytokines?

A

Dysbiosis

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42
Q

Can consider periodo as an extra-articular source increased auto antibodies in what disease?

A

Rheumatoid arthritis

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43
Q

Perio and precancerous cells can lead to what type of cancer?

A

Colorectal

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44
Q

Travels through blood and infects tumor cells via attachment to a sugar molecule on their surface

A

Fusobacterium nucleatum

45
Q

Associated with periodo, tonsillitis, appendicitis and preterm labor

A

Fusobacterium nucleatum

46
Q

Infection in tumor cells of pancreatic , esophageal or colorectal cancer increases resistance to chemo and causes an inflammatory cytokine storm, which can lead to metastasis of the cells accelerating progression

A

Fusobacterium nucleatum

47
Q

Previously Aggressive
Localized Juvenile Periodontitis (LJP)
Refractory Periodontitis

A

World Task Force diagnosis

48
Q

-Aggregatibacter actinomycetemcomitans
-Inherited defect of neutrophil functions including: impaired chemotaxis, phagocytocis, and killing of bacteria
-Possibly due to a lytic enzymatic release against pathogens of primed neutrophils to debridement so less remains for chemotaxis and defense
-Strong genetic component
-Smoking component as well

A

LJP

49
Q

Identified initially w/ Pubescent Females of African Descent but some studies afterwards found a stronger genetic component in
Caucasians

A

LJP

50
Q

Some immunological marker differentiation

A

LJP

51
Q

Responds well to treatment if caught in time

A

LJP

52
Q

First molars and any incisor typically but anywhere is possible if generalized

A

LJP

53
Q

Know specificity vs sensitivity definitions

A
54
Q

BOP has _______ specificity, _______ sensitivity

A

high specificity; low sensitivity

55
Q

What accounts for 1/3 of all dental emergency visits and is very painful?

A

Perio abscess

56
Q

What disease?

Edematous
Lymphadenopathy
Fever
Increased tooth mobility/extrusion
Exudate/suppuration
Isolated deep PDs

A

Perio abscess

57
Q

The epithelial tissues can reattach to the root of the tooth, whereas bacteria and debris remain in the apical aspect of the pocket. With the coronal portion of the pocket occluded, drainage is impaired and an abscess may result

A

Perio abscess

58
Q

What is mandatory when diagnosing a perio abscess?

A

Differential diagnosis

59
Q

What is the tx for a perio abscess?

A

Drainage via socket or open SRP

60
Q

What medications are prescribed for a perio abscess?

A

PenVK 500 mg
Doxycycline 100 mg

61
Q

What 2 lesions should you rule out before diagnosing a perio abscess?

A

Endo PA lesion
Lateral canal lesion

62
Q

Pulp testing 15% due to perio abscess

A
63
Q

What are the 3 complications of perio abscesses?

A

Cellulitis
Airway patency
Sinus infections

64
Q

What is imperative after treating a perio abscess?

A

Post-op care

65
Q

What is the post-op care after treating a perio abscess?

A

RTC 1-2 days, then weekly to evaluate

66
Q

Which 2 bacteria are involved in perio abscess?

A

P gingivalis
P intermedia

67
Q

A biopsy of a perio abscess reveals invasive ________ present in pocket epithelium into adjacent CT

A

fungi

68
Q

____________ microbes predominate perio abscesses

A

Anaerobic

69
Q

If your pt has 3mm of CAL, but pocket depths are 3mm or less, do they have active perio disease?

A

No

70
Q

What are the 2 necrotizing perio diseases?

A

Necrotizing ulcerative gingivitis (NUG)
Necrotizing ulcerative perio (NUP)

71
Q

Both NUG and NUP may be manifestations of underlying systemic problems such as what?

A

HIV

72
Q

What factors, other than systemic considerations, appear to be predisposed to the development of NUG and NUP?

A

Cig smoking
Emotional stress

73
Q

What are the clinical signs and symptoms of NUG and NUP?

A

Interproximal necrosis/ulceration
History of soreness/bleeding when brushing/eating
Pseudomembrane covering a “punched out” papilla

74
Q

The extent and degree of involvement of NUG and NUP varies considerably from…

A

One papilla to entire gingiva

75
Q

NUG or NUP?

On the basis of clinical findings
Onset of the disease is sudden
Severe pain around the teeth and gingiva (“My
entire mouth hurts”)

A

NUG

76
Q

NUG or NUP?

Pain is more intense around the sites of ulceration (elicited upon brushing or when eating)
Gingiva bleeds and most often spontaneously
Spicy foods, hot or cold drinks or alcoholic beverages may be intolerable

A

NUG

77
Q

Also called “Trench mouth” or Vincent’s Disease

A

NUG

78
Q

What are the 4 systemic signs and symptoms of NUG?

A

Lymphadenopathy
Fetor oris
Fever
Malaise

79
Q

What are the following a differential diagnosis of?

Acute gingivitis
Primary herpetic gingivostomatitis
Recurrent apthous stomatitis
Desquamative gingivitis
Infectious mononucleosis
Streptococcal or staphylococcal pharyngitis
Acute leukemia
Agranulocytosis
Secondary/Tertiary stage syphilis

A

NUG

80
Q

What disease?

Fusospirochetal disease always appears to be superimposed onto existing tissue damage

A

ANUG

81
Q

What disease?

Concluded that neither spirochetes nor fusobacteria could be excluded as the etiologic agents

A

ANUG

82
Q

What 4 zones contain spirochetes in ANUG?

A

Bacterial zone
Neutrophil rich zone
Necrotic zone
Spirochetal infiltration zone

83
Q

Which zone of ANUG?

Most superficial zone, consists primarily of a mass of bacteria of various sizes and shapes, including a few spirochetes

A

Bacterial zone

84
Q

Which zone of ANUG?

Underlies the Bacterial zone

A

Neutrophil rich zone

85
Q

Which zone of ANUG?

Many leukocytes with a marked predominance of neutrophils; spirochetes found btwn leukocytes

A

Neutrophil rich zone

86
Q

Which zone of ANUG?

Contains disintegrating tissue cells, many spirochetes of the intermediate and large type and a few other bacteria which are probably fusiforms

A

Necrotic zone

87
Q

Which zone of ANUG?

Tissue components appear well preserved, but are infiltrated with spirochetes of various sizes; no other bacteria are found in this zone

A

Spirochetal infiltration zone

88
Q

Spirochetes can be found in ___________ tissue ahead of other bacterial types

A

non-necrotic

89
Q

T/F: There is no marked difference in the relative infectivity of bacterial debris, injected into experimental animals, from the normal gingival sulcus, the periodontal pocket, or areas of papillary necrosis associated with ANUG

A

True

90
Q

What is responsible for the development of ANUG?

A

Decreased host resistance

(rather than increased bacterial virulence)

91
Q

What are the 8 local predisposing factors of ANUG?

A

Gross neglect
Overcrowding
Recent exts
Food stagnation
Mouth breathing
Calculus
Smoking
Emotional stress

92
Q

T/F: Fatigue and local trauma, along with physical debility and lowered resistance play a role in ANUG

A

True

93
Q

What is an important etiologic factor of ANUG?

A

Pre-existing gingivitis

94
Q

What is directly correlated to the severity of ANUG?

A

Tobacco

95
Q

What is the characteristic flora of NUG directly related to?

A

Altered host response

96
Q

Very young pts with measles, protozoal infection, and malnutrition have increased risk of what?

A

NUG

97
Q

How do you treat NUG?

A

Control acute bacterial phase
Educate pt in plaque control
Eliminate predisposing factors
Early + vigorous local tx during acute phase
Antibiotics only when systemic complications prevail

98
Q

T/F: When treating NUG, drugs should never be considered a substitute for scaling and debridement

A

True

99
Q

What should you do at the first visit when seeing a pt with NUG?

A
  1. Remove as much calc, plaque, and debris as possible with ultrasonic instrument
  2. Educate pt how to remove plaque with new toothbrush
  3. Prescribe ABs if fever or lymphadenopathy
  4. Instruct specific home care
100
Q

What is the home care for NUG?

A
  1. Rinse w/ 0.12% CHX 2x/day
  2. Soft, bland diet
  3. Drink lots of water
  4. No smoking or drinking
  5. Rest
  6. Rinse mouth after eating
  7. Brush teeth
  8. Return to office in 24 hrs
101
Q

What should you do at the 2nd visit when seeing a pt with NUG?

A
  1. Check OH, review plaque control
  2. Continue removing calc, plaque, debris
  3. Careful SRP and flush w/ warm water
  4. Polish
  5. Tell pt to return after 24-48 hrs
102
Q

What should you do at the 3rd visit when seeing a pt with NUG?

A
  1. Check OH, review plaque control
  2. Continue removing calc, plaque, debris
  3. If tissues haven’t responded -> evaluate for systemic factors and refer for med consult; continue seeing pt every 24-48 hrs
  4. If you see improvement, tell pt to return in 7-10 days
103
Q

What should you do at the 4th visit when seeing a pt with NUG?

A
  1. Check OH, review plaque control
  2. Continue removing calc, plaque, debris
  3. Reinforce OH
  4. Definitive SRP
  5. Polish
  6. Evaluate for further perio tx
103
Q

Self-limiting disease that usually resolves within 10 days to two weeks

A

NUG

104
Q

If symptoms persist, a complete medical evaluation (physician referral) is indicated for possible systemic factors

A

NUG

105
Q

What do you do in the subsequent visits after treating a pt with NUG?

A
  1. Correction of residual defects
  2. Reinforce OH
  3. Refer for psych or med consult if disease recurs regularly
106
Q

Which diseases?

The most severe inflammatory periodontal diseases caused by plaque bacteria
Run an acute course
Rapidly destructive and debilitating

A

Necrotizing gingivitis (NG)
Necrotizing perio (NP)
Necrotizing stomatitis (NS)

107
Q

Page 42

A