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Perio Exam 2 > Sweep 2.2 > Flashcards

Sweep 2.2 Flashcards

1
Q

Candidosis-

A

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

C.albicans is frequently isolated from the subgingival flora of patients with severe periodontitis.

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2
Q

Candidosis-

lesions

A

Painless or slightly sensitive
Red and white lesions
Lesions can be scraped or separated from mucosa

Cancer patients receiving high dose radiation or
chemotherapy
Patients who are using several different antibiotics
over a period of several weeks or months
Diabetic patients
Women who develop vaginal candidiasis
Pregnancy and the use of contraceptives

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3
Q

Most clinical charateristic of gingival candidal infections is

A

redness of the attached gingiva, often associated with granular surface.

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4
Q

Different types or oral mucosal manifestations:

A

Pseudomembraneous (whitish patches that can be wiped off)
Erythematous (red, associated with pain)
Plaque type (whitish plaque that cannot be removed; need to differentiate from oral leukoplakia)
Nodular (slightly elevated nodules of white or reddish color)

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5
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.
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6
Q

LGE: Linear gingival erythema-

- Gingival manifestation of

A

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

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7
Q

LGE:

- Does not respond well to

A

improved oral hygiene or to scaling.

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8
Q

LGE: - A disproportion between

A

inflammation and plaque accumulation.

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9
Q

LGE: Treatment:

A
  • Conventional therapy plus chlorhexidine 0.12% rinse

- Antimycotic therapy if Candida is detected.

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10
Q

Histoplasmosis-

A
  • Granulomatous disease caused by Histoplasma capsulatum *
    • Acute and chronic pulmonary histoplasmosis and a disseminated form… Immunocompromised patients.
    • Any area of the oral mucosa (mainly tongue).
    • Nodular or papillary and later may become ulcerative type of lesions with pain.
      Diagnosis: Clinical view and histopathology, systemic manifestations
      Treatment: Systemic antifungal therapy
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11
Q

Hereditary gingival fibromatosis-

Possible mechanism(s):

A

TGF-1 favor the accumulation of ECM.
May be located on chromosome 2 in human.
[ Defect in the Son of Sevenless-1 gene on chromosome 2p21-p22]

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12
Q

LAP: Most frequently between

A

puberty & 20yrs of age.

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13
Q

LAP: Pattern:

A

Localized CAL in first molars/incisors (at least 1 first molar must be affected).

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14
Q

LAP: Distribution: no more than

A

2 teeth other than first molars and incisors are affected .

CAL is inconsistent with amount of plaque & calculus.

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15
Q

LAP: Relatively less intense

A

gingival inflammation.

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16
Q

LAP: Robust

A

serum antibody response (IgG2).

Self limiting

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17
Q

GAP: Distribution: AT least 3 permanent teeth other than

A

1st molars & incisors.

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18
Q

GAP: Pronounced episodic nature of the

A

destruction of attachment/bone.

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19
Q

gAP: Relatively intense

A

gingival inflammation.

Poor serum antibody response.

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20
Q

A.a is associated with

A

LAP - particularly JP2 clone serotype

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21
Q

A.a

A

Facultative anaerobe, nonmotile.

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22
Q

A.a can

A

translocate across JE, invade CT

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23
Q

A.a Virulence factors:

A 
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
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24
Q

P. gingivalis:

A

Anaerobe, nonmotile, G-.

25
P. gingivalis | Virulence factors:
Proteinases: Gingipains, Collagenases LPS: activates cells to produce PGs, IL-1β, TNF-α Inibits IL-8: ↓ chemotaxis of PMNs.
26
LAP host response
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 .
27
LAP: treatment
Full mouth SRP in adjunct with systemic antibiotics. Amoxicillin + Metronidazole Ciprofloxacin + Metronidazole Possible periodontal surgery. Meticulous periodontal supportive therapy.
28
Primary occlusal trauma
``` Excessive force (e.g.: “high restoration”) Normal periodontium ```
29
Secondary occlusal trauma
Normal (or excessive forces) | Applied to a weakened periodontium
30
Fremitus:
a vibration perceptible on palpation; in dentistry, a vibration palpable when the teeth come into contact
31
Side effects of occlusal forces being too great (controversial)
``` Infrabony pockets (controversial) Butttressing Bone ```
32
Radiograph - occlusal trauma
Some of the changes may represent adapation | Some may be due to extension of inflammatory periodontal disease without occlusal trauma as a factor
33
Widened PDL Space and/or Thickened Rad. Lamina Dura
from occlusal trauma
34
Ang. bone loss & Furcations
Controversial | May purely be due to tooth and bony anatomy and the progression and the of inflammatory periodontal disease
35
Co-destruction Theory (Glickman):
Occlusal trauma may be a co-destructive factor that alters the severity and pattern of inflammatory periodontal disease
36
Advancing Plaque Front Theory (Waerhaug):
Occlusal trauma has no role in the severity and pattern of inflammatory periodontal disease progression
37
TFO without Periodontitis
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
38
Models For Role of Occlusal Trauma
Trauma From Occlusion Without Periodontitis Trauma From Occlusion with Periodontitis: But No Co-destruction Trauma From Occlusion With Periodontitis: Co-destruction Occurs
39
Subcrestal (infrabony) lesion with no TFO:
No co-destruction
40
Subcrestal periodontitis with TFO- two lesions merge :
: CO-DESTRUCTION
41
Subcrestal (infrabony) perio. with adaptation:
Maybe CO-DESTRUCTION
42
Occlusal therapy is especially indicated prior to
periodontal regenerative therapy
43
Occlusal adjustment is not justified in the absence of
periodontal disease as a preventive measure
44
Shape of the gingival margin: In healthy gingiva….
- Scalloped with gingiva filling interdental spaces ( presence of papilla).
45
Shape of the gingival margin: With inflammation…
- Knife edge gingival adaptation or loose gingival margins | - In some cases, clefts (Stillman’s) or festoons (McCall’s) may develop
46
Gingival enlargement
Clinically deep red lesions with soft, friable, smooth, shiny surface and bleeding tendency Also, relatively firm, resilient and pink lesions with greater fibrotic component, abundant fibroblasts and collagen fibers
47
Pyogenic granuloma of pregnancy- Commonly arises from the ---------- and has a ------------.
proximal gingival tissues pedunculated base The usual presentation is in the second or third trimester of pregnancy. A highly vascularized mass of granulation tissue.
48
Differential diagnosis of NUG and primary herpetic | gingivostomatitis (PHS).
Etiology….. Bacteria (NUG), Herpes simplex virus (PHS) * Symptoms… Ulceration and necrotic tissue, yellowish white plaque (NUG) Multiple vesicles which burst leaving small round fibrin covered ulcers (PHS) * Duration…. 1-2 days if treated (NUG) 1-2 weeks (PHS) * Contagious… No (NUG) Yes (PHS)
49
NUG/ANUG
Confined in interdental papillae and marginal gingiva. Characterized by rapid onset of gingival pain, interdental gingival necrosis , and bleeding. Affected young adults, associated with cigarettes smoking and stress.
50
Clinical signs of NUG
Severe Pain is the chief complaint of the pt. Ulceration covered by a yellowish – white or grayish slough which is termed “Pseudo membrane”. Necrotic interdental papillae: Punched out appearance. Bleeding either spontaneously or upon gentle manipulation.
51
Etiology & Pathogenesis of NPD | Aggressive causative agents
``` Bacteria -Spirochetes (Treponema) -Fusobacterium -P. intermedia Virus -Human cytomegalovirus(CMV) -HIV ```
52
NPD Host factors
``` Immunosuppression Systemic disease (HIV) Malnutrition Pre-existing gingivitis, poor oral hygiene, history of NPD Psychological stress, lack of sleep Smoking ```
53
Histopathology of NPD
Necrosis of epithelium and superficial layers of the connective tissue. Hyperemic CT with engorged capillaries and dense infiltrations of PMNs.
54
Periodontitis-related Abscess
``` Exacerbation of chronic lesion Untreated patients Maintenance patients (recurrent infection) Post-therapy Abscess Following SRP (calculus) Following surgical therapy (calculus, foreign bodies) Post-antibiotic Abscess Super-infection ```
55
Non-Periodontitis-related Abscess
``` Foreign body impaction Oral hygiene devices Food particles Root morphology alterations Iatrogenic (endodontic perforation) External root resorption Cemental tears ```
56
Periodontal Abscess - Therapy
``` Acute lesion management Irrigation with antiseptics Drainage When present, removal of foreign body Debridement OHI Antibiotics Review after 24-48 hours; a week later, the definitive treatment should be carried out. Definitive treatment ```
57
Sensory feedback through receptors localized within pdl
(viscoelasticity)
58
Sensory feedback through receptors localized within bone
(elasticity)…
59
Implant loading time depends on:
- Primary stability of the implant - Implant design - Restorative design - Presence/absence of risk factors

Perio Exam 2 (20 decks)

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