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Perio Exam 2 > Perio sweep 1 > Flashcards

Perio sweep 1 Flashcards

1
Q

Gingival Diseases Modified by Systemic Factors Associated with:

A

the endocrine system (endocrinotropic)
blood dyscrasias
medications
nutrition

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2
Q

Endocrinotropic Gingival Diseases

A 
puberty-associated gingivitis
menstrual cycle-associated gingivitis
pregnancy-associated gingivitis
pregnancy-associated pyogenic granuloma
diabetes mellitus-associated gingivitis
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3
Q

menstrual cycle-associated gingivitis –

A

nonsense, they looked at crevicular fluid flow, but clinically you won’t really see this.

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4
Q

Gingival Disease Associated with Blood Dyscrasias:

Leukemia-associated gingivitis

A

gingival lesions are primarily found in acute leukemia

reductions in dental plaque can limit the severity of lesion

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5
Q

Gingival Disease Modified by Nutrition

Ascorbic acid-deficiency gingivitis

A

Malnourished individuals have a compromised host defense system which may make individuals susceptible to infectious diseases

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6
Q

The precise role of nutrition in periodontal diseases

A

remains to be elucidated.
Human studies have failed to show a relationship between nutrition and periodontal diseases

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7
Q

Chronic Periodontitis aka

A

formerly adult perio

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8
Q

Chronic Periodontitis

Clinical manifestations

A 
Pocket formation
Loss of attachment
Bleeding/suppuration
Bone loss
Tooth mobility and drifting
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9
Q

Number one difference between gingivitis and other periodontal disease is

A

attachment loss.

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10
Q

Chronic Periodontitis: ———- frequent finding

A

subgingival calculus

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11
Q

Chronic Periodontitis usually ——– progression

A

slow

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12
Q

Chronic Periodontitis: Can be associated with

A

local predisposing factors (e.g., tooth-related) – diabetes ex

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13
Q

Chronic Periodontitis: extent, severity:

A 
extent
localized < 30% 
generalized (>30%)
severity
slight - 1 to 2 mm CAL
moderate - 3 to 4 mm CAL
severe - > 5 mm CAL
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14
Q

Aggressive Periodontitis formerly known as

A

prepubertal periodontitis
localized juvenile periodontitis
generalized juvenile periodontitis
early-onset periodontitis

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15
Q

Aggressive perio Can be identified as either:

A

localized

generalized

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16
Q

Aggressive Periodontitis common features:

A

systemically healthy

rapid attachment loss and bone destruction

familial aggregation

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17
Q

Aggressive Periodontitis secondary features:

A

generally but may not be universally present

microbial deposits are inconsistent with the amount of periodontal destruction

elevated Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis

phagocyte abnormalities

hyper-responsive macrophage phenotype (e.g., elevated levels of PGE2 and IL-1b

progression may be self-arresting

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18
Q

Localized Aggressive Periodontitis ———- onset

A

Circumpubertal

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19
Q

LAP: ———– to infecting agents

A

Robust serum antibody response

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20
Q

LAP: Localized first molar/incisor presentation

interproximal attachment loss on at least

A

2 permanent teeth
one of which is a molar
involving no more than 2 teeth other than first molars and incisors

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21
Q

Generalized Aggressive Periodontitis characteristics

A

Poor serum antibody response to infecting agents
Pronounced episodic nature of destruction of attachment and bone
Generalized interproximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors.

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22
Q

Perio Associated with hematologic disorders

A

acquired neutropenia

leukemias

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23
Q

Perio Associated with genetic disorders

A

Familial & cyclic neutropenia
Down syndrome
Leukocyte adhesion deficiency syndrome
Papillon-Lefèvre – collagen defect. 1/1000000

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24
Q

Trisomy and perio

A 
Down syndrome
autosomal inherited trisomia of chromosome 21
frontal prominence/mesial epicanthus
periodontium
severe inflammation
accelerated attachment loss
PMN chemotaxis and killing defects
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25
Q

Papillon-Lefèvre syndrome

autosomal recessive hereditary disorder

A

rapid periodontal destruction around primary and permanent teeth which occurs before puberty

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26
Q

Chediak-Higachi syndrome

autosomal recessive hereditary disorder

A

rapid periodontal destruction around primary and permanent teeth which occurs before puberty

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27
Q

Ehlers-Danlos syndrome (types IV & VIII)

autosomal dominant hereditary disorder

A

aggressive periodontitis (primary and permanent dentitions); fragility of gingiva, excessive hemorrhage

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28
Q

NPD —– is why patients come in

A

pain. have punched out papilla.

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29
Q

NPD: Early Clinical Signs

A

Necrotic lesion of the papilla initially then progressing to gingival margin.
Punched-out appearance
Spontaneous bleeding
Pain

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30
Q

NPD: Advanced Lesion

A

Lack of deep pockets
Merging of papillary and marginal involvement
Characteristic foetor
Central necrosis results in crater formation
Involvement of periodontal ligament and alveolar bone (NUG  NUP)

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31
Q

NUP: Involvement of palatal mucosa ——->

A

 necrotizing stomatitis

32
Q

NUP: Typically related to

A

severely compromised immune system (HIV infection, malnutrition

May develop into life-threatening situation

33
Q

NUP: Extra-oral involvement of

A

regional lymph nodes

34
Q

NPD other findings systemically and orally

A

Fever and malaise. Moderate elevation of temperature can be observed
Poor oral hygiene.
White membrane of desquamated cells, bacteria, saliva proteins.
Membrane can be easily removed

35
Q

A.a is associated with

A

LAP

36
Q

A.A associated with LAP: Particularly

A

JP2 Clone , serotype b

37
Q

A.a:

A 
Facultative anaerobe, nonmotile.
Virulence factors:
Leukotoxins: kills PMNs and MΦ
LPS: activates cells to produce PGs, IL-1, TNF-
Collagenases: degrades collagen fibers 
Immunosuppressive factors : 
Lymphocyte supprressing factors
Chemotactic suppressing factors

Translocate across the JE
Invade the CT

38
Q

P. gingivalis

A

Anaerobe, nonmotile, G-.

39
Q

P. Gingivalis: Virulence factors:

A

Proteinases: Gingipains, Collagenases
LPS: activates cells to produce PGs, IL-1β, TNF-α
Inibits IL-8: ↓ chemotaxis of PMNs.

40
Q

Proposed inheritance mode for LAP:

A

autosomal dominant.

41
Q

LAP host response

A

Impaired neutrophil function (chemotaxis and phagocytosis.)
Significantly higher levels of prostaglandin E2 in GCF.
Antibody against A.a is extremely high(Levels in sulcus fluid higher than in peripheral blood)
High titers and high avidity of IgG2 in LAP.
Low levels of Ab against P.g in GAP patients .

42
Q

Community Periodontal Index of Treatment Needs (CPITN)

A

Introduced by World Health Organization
Major advantages include simplicity, speed, reproducibility and uniformity
Can be used as part of a global surveillance system to compare periodontal health in differing countries
Provides information concerning the type of disease and therefore the extent of therapy

43
Q

CPITN: Mouth divided into

A

sextants defined by tooth numbers:

1–5, 6–11, 12–16, 17–21, 22–27, 28–32

44
Q

CPITN: Index is calculated by…

A

teeth in each sextant probed and pocket depth, subgingival calculus and bleeding response determined

45
Q

CPITN coding:

A

0 = patient keeps doing what they’re doing.
1 = BOP. Some inflammation – plaque probably, maybe calculus. Prophy, OHI, 6 month recalls.
2 = remove plaque retentive factor (amalgam overhang). In many cases, perio case treatment is not perio treatment. Smooth down overhang.
3 = Lose plaque. Deepened sulcus, maybe a pocket, once you get score of 3, you don’t know cause. Drop PSR probe and start perio evaluation. Treatment = full comprehensive perio eval.
4 = Pocket 6mm or more
X – Excluded sextant (not shown)
9 – Not recorded (not shown)

46
Q

CPITN has

A

This has limited use in children.

47
Q

There are two major forms of periodontal diseases.

A

Gingival diseases

Destructive periodontal diseases

48
Q

Periodontal diseases are highly prevalent throughout the world.
Majority of studies:

A

10 -20% for advanced levels of periodontitis

49
Q

Periodontal health affects approximately —- of population.

A

10%

50
Q

Candidosis-Candida species isolated from the mouth:

A

C.albicans, C.glabrata, C.krusei, C.tropicalis, C. parapsilosis and C. guillermondii.

51
Q

Oral carriage of C.albicans in healthy adults:

A

3-48%.

52
Q

Candidiosis associated with

A

Reduced host defense {immunosuppressed individuals, infant and adult who has been on antibiotic therapy for some time}

53
Q

C.albicans is frequently isolated from the

A

subgingival flora of patients with severe periodontitis.

54
Q

Candidosis-

Diagnosis:

A

A culture on Nickersons medium at room temp.
Microscopic examination of a smear of the material
scraped from the lesion and stained.

55
Q

Candidosis: Treatment:

A

The use of the antimycotic/antifungal agents

[example: Nystatin given as a mouthrinse or systemically]

56
Q

In otherwise healthy patients, oral candidosis rarely manifests in the

A

gingiva. This is suprising considering that C albicans is frequently isolated from the subgingival flora of patients with severe periodontitis.

57
Q

Most clinical charateristic of gingival candidal infections is

A

redness of the attached gingiva, often associated with granular surface. There are different types:
Pseudomembraneous, erythematous, plaque type, nodular…

58
Q

Pseudomembraneous shows

candisosis

A

patches which can be whiped off

59
Q

Erythematous are

candisosis

A

intensely red usually associated with pain,

60
Q

candisosis

Plaque type has

A

whitish plaque that cannot be removed by whiping…

61
Q

Candidosis; Diagnosis can be completed by

A

culture, smear and biopsy

62
Q

Linear gingival erythema-

-

A

Distinct linear erythematous band limited to the free gingiva.
- Lack of bleeding.
Positive for C.albicans by culture:
50% of HIV associated gingivitis sites,
26% of unaffected sites of HIV seropositive patients, 3% of healthy sites of HIV negative patients.

63
Q

Linear gingival erethema Treatment generally include

A

conventional tx+chlorhexidine rinse for 3 months.

64
Q

Linear gingival erythema-

- Gingival manifestation of

A

immunosuppression
characterized by a distinct linear erythematous band
limited to the free gingiva

65
Q

Linear gingival erythema: - Does not respond well to

A

improved oral hygiene or to scaling.

66
Q

Linear gingival erythema: - A disproportion between

A

inflammation and plaque accumulation.

67
Q

Linear gingival erythema: Treatment:

A
  • Conventional therapy plus chlorhexidine 0.12% rinse

- Antimycotic therapy if Candida is detected.

68
Q

Hereditary gingival fibromatosis-

-

A

Diffuse gingival enlargement.

- Disease entity or a part of a syndrome.
 (example: hypertrichosis, mental retardation,        epilepsy, hearing loss, growth retardation, abnormalities of extremities)
- May interfere with or prevent tooth eruption.
69
Q

Hereditary gingival fibromatosis: Possible mechanism(s):

A

TGF-1 favor the accumulation of ECM.

May be located on chromosome 2 in human

70
Q

Hereditary gingival fibromatosis (HGF) is a rare gingival lesion that presents as

A

localized

or generalized enlargement of the attached gingiva.

71
Q

Type I reactions (immediate Type),mediated by

allergy

A

IgE,

or

72
Q

Type IV reactions

allergy

A

(delayed type) mediated by T-cells.

[12-48 hrs following contact with allergen]

73
Q

Allergies to:

Dental restorative materials

A

(type IV, contact allergy)

74
Q

Allergies; A diffuse fiery red edematous gingivitis sometimes with

A

ulcerations or whitening.

75
Q

Physical traumatic lesions-

Hyperkeratosis,

also,

A

a white leukoplakia-like, frictional keratosis.

Gingival laceration resulting in gingival recession.

Traumatic ulcerative gingival lesion.
(brushing and flossing techniques)
76
Q

TFO without Periodontitis

A

Injury results in acute (not plaque associated) inflammation
PDL collagen destruction
Cementum resorption
Bone loss
No attachment loss
Adaptation may occur: tooth may become mobile, but no further injury

Perio Exam 2 (20 decks)

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