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Perio Exam 2 > Perio sweep 1.2 > Flashcards

Perio sweep 1.2 Flashcards

1
Q

Gingivitis around implants =

A

Peri-mucositis

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2
Q

Characteristics common to all gingival diseases:

A

1- Signs and symptoms limited to the gingiva.

2- The presence of dental plaque.

3- Clinical signs of inflammation.

4- Clinical signs and symptoms associated on a periodontium with no attachment loss or on a stable but reduced periodontium.

5- Reversibility of the disease by removing the etiology.

6- Possible role as a precursor to attachment loss.

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3
Q

Near Infrared (NIR) Spectroscopy

A

Measure of oxygen saturation of the tissues
The wavelength region 500 to 600 nm is dominated by the absorption from oxygenated hemoglobin (HbO2) and deoxygenated hemoglobin (Hb)
Tissue oxygenation at periodontitis sites significantly ↓ as compared to gingivitis and healthy control sites

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4
Q

Saliva test:

A

Type and concentration of specific periodontal pathogens
- Apply DNA PCR – identify specific periodontal pathogens
Genetic susceptibility to periodontitis in individuals
- Test genetic variation: over-expression of IL-1α and IL-1β

These tests identify general risk factors for the development of periodontal diseases, but fail to determine when periodontal destruction will occur
NOT being able to specifically predict periods of disease activity

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5
Q

Salivary Occult Blood Test (SOBT) –

A

available in Japan
A poor periodontal status: Subjects having ≥15% of teeth with BOP or ≥ 1 tooth with PD ≥ 4mm
A paper strip containing gold-labeled anti-human hemoglobin monoclonal antibody was dipped into saliva sample (Positive: ≥ 2 μg/ml human hemoglobin)
Sensitivity:0.72; Specificity: 0.52

After swishing with three milliliters of distilled water for 10 seconds, the mixture is spit into a cup and the Perioscreen test strip is dipped into the saliva sample. The colloidal gold-labeled antibody dissolves in the salvia sample and if blood is present, an immune complex is formed and moves up the test strip by capillary action, resulting in a magenta line.

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6
Q

The SOBT may offer a simple screening method for periodontal status when a

A

thorough periodontal examination is not possible, although it is not sufficiently specific to be a reasonable substitute for a periodontal examination

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7
Q

Gingivitis associated with dental plaque only

A

w/o other local contributing factors

w/ other local contributing factors

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8
Q

> Gingival diseases modified by systemic factors

A 
Associated w/ endocrine system
-Puberty associated gingivitis
-Menstrual cycle associated gingivitis
-Pregnancy associated gingivitis
-Diabetes mellitus associated gingivitis
Associated w/ blood dyscrasias
-Leukemia associated gingivitis
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9
Q

> Gingival diseases modified by medications

A

Gingival enlargements

Oral contraceptive associated gingivitis

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10
Q

> Gingival diseases modified by malnutrition

A

Ascorbic acid deficiency gingivitis

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11
Q

Normal gingival color:

A

“coral pink”+ pigmentation

[tissue’s vascularity and overlying epithelial layers]

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12
Q

Inflammed gingiva:

A

red

[increased vascularization and decreased epithelial keratinization]

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13
Q

Severly inflammed gingiva:

A

red and cyanotic
[vascular proliferation and reduction in keratinization +
venous stasis]

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14
Q

Changes start at

A

interdental papillae and gingival margin and spread to the attached gingiva.

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15
Q

Gingival bleeding: With increasing inflammation:

A

Dilation and engorgement of the capillaries

Thinning or ulceration of the sulcular epithelium

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16
Q

Chronic or recurrent bleeding,

A

provoked by trauma.

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17
Q

Spontaneous bleeding occurs in

A

acute/severe gingival disease and may be related to systemic health problems.

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18
Q

With inflammation:

A
  • Increase in extracellular fluid and exudate,
    • Degeneration of connective tissue and epithelium,
    • Engorged connective tissue and thinning of epithelium.
      Soft, swollen (edema), friable.
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19
Q

In severe gingival disease:

A

Sloughing with grayish flake-like debris (necrosis)

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20
Q

Chronic inflammation can induce

A

fibrosis and epithelial proliferation….

firm leathery consistency.

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21
Q

Healthy gingiva…

A

Dull surface texture with stippling present in some cases.

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22
Q

With inflammation:

loss of

A

stippling,

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23
Q

smooth and shiny …if

A

exudative changes occur,

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24
Q

firm and nodular …if

A

fibrotic changes occur.

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25
Q

shape healthy gingiva….

A
  • Scalloped with gingiva filling interdental spaces ( presence of papilla).
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26
Q

Shape of gingiva With inflammation…

A
  • Knife edge gingival adaptation or loose gingival margins

- In some cases, clefts (Stillman’s) or festoons (McCall’s) may develop

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27
Q

Perio Primary etiologic factor =

A

Bacterial plaque

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28
Q

Secondary etiological factors =

A

local factors

* Calculus
* Marginal deficiencies in restorations and rough surfaces
* Malocclusion
* Tooth/root anomalies
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29
Q

Bio width

A

“A minimum dimension of 3 mm coronal to the alveolar crest … to permit healing and proper restoration.”

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30
Q

Bio width: “Intracrevicular restorative margins” at sites of

A

insufficient gingival (or marginal tissue) width and/or thickness ….

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31
Q

Periodontitis starts with

A

gingivitis

32
Q

The return of inflammation to sites treated for

periodontitis is .

A

common

33
Q

The recurrent inflammation may be confined to the

A

gingival tissues and may not cause further attachment

loss. This is still diagnosed as “recurrent periodontitis

34
Q

Gingival diseases modified by endocrine factors

A

Need to have dental plaque !!!

Pregnancy associated gingivitis
Puberty associated gingivitis
Menstrual cycle associated gingivitis

35
Q

Pregnancy associated gingivitis:

A

Microbiota …. Characteristic of gingivitis.

Exaggerated localized host response modulated by levels of endogenous hormones (androgens, estrogens and progesterone).

Changes often appear during 2nd trimester and regress upon parturition.

36
Q

Puberty associated gingivitis-

A

Localized host response mediated by high levels of hormones

(estrogens,testosterone

37
Q

Puberty associated gingiviits: ——- can be a secondary factor

A

mouth-breathing.

38
Q

Menstrual cycle associated gingivitis-

A

Clinically detectable changes do not seem to be
associated with the menstrual cycle.

An increase in GCF (Gingival Crevicular Fluid)
by 20% has been described.

39
Q

Pyogenic granuloma of pregnancy-

A

Commonly arises from the proximal gingival tissues and has a pedunculated base.

The usual presentation is in the second or third trimester of pregnancy.

A highly vascularized mass of granulation tissue.

40
Q

Gingival diseases modified by systemic conditions-

A

Diabetes mellitus …Type I and II

Leukemias and other blood dysplasias.

Acute myeloid leukemia associated with gingival changes.

Persistent unexplained gingival bleeding may indicate underlying thrombocytopenia.

Cyclic neutropenia (14-36 days cycle) … Ulcerations

41
Q

Gingival diseases modified by medications-

3 commonly used drug types that are associated with
gingival overgrowth:

A

Anticonvulsants (Phenytoin sodium or epinutin)
Immunosuppressant (Cyclosporin A)
Calcium channel blocking agents (Nifedipine).

42
Q

Necrotizing Ulcerative Gingivitis (NUG)

A

Adolescents or young adults, may be smokers and individuals often with psychological stress.

Pain, ulceration and necrosis of the interdental papillae, bleeding.

Differential diagnosis with primary herpetic gingivostomatitis.

The resolution of the disease is often required systemic antibiotic.

43
Q

NUG:

Predisposing factors:

A
  • Systemic diseases like ulcerative colitis, blood dyscrasias and nutritional deficiency states.
  • Abnormalities of white blood cell function.
  • Patients suffering from AIDS

Associated with periodontal attachment loss.
May progress to Noma or cancrum oris.

44
Q

Differential diagnosis of NUG and primary herpetic

gingivostomatitis (PHS).

A
  • 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)
45
Q

Necrotizing Periodontal Diseases (NPD)

A

Necrotizing Ulcerative Gingivitis (NUG)

Necrotizing Ulcerative Periodontitis (NUP)

46
Q

Necrotizing Ulcerative Gingivitis

A

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.

47
Q

Clinical signs of NUG

A

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.

48
Q

Necrotizing Ulcerative Periodontitis (NUP)

signs

A 
Necrosis of papilla (“punched-out”)
Pain (chief complaint)
Bleeding
-Other
--“pseudomembrane” (=sloughed material)
---Halitosis (foetor ex ore)
Attachment loss
49
Q

Other findings of NPD

A

Oral hygiene usually poor, painful when brushing.
Swelling of regional lymph nodes may occur.
Usually confined to the submandibular lymph nodes
Cervical lymph nodes may also be involved.
Fever and malaise are not consistent characteristics.
Increased salivation.

50
Q

Epidemiology of NPD

young adults

A 
Industrialized countries
Prevalence between 2% and 7% (1960)
Higher under certain conditions: smoking and stress.
Developing countries
Much higher prevalence
51
Q

Epidemiology of NPD

immunocompromised patients

A

Prevalence between 1% and 28%.

Significantly decreased after anti-retroviral therapy.

52
Q

Etiology & Pathogenesis of NPD

A 
Bacteria
Spirochetes (Treponema)
Fusobacterium
P. intermedia
Virus
Human cytomegalovirus(CMV)
HIV
53
Q

NPD: Host factors

A 
Immunosuppression
-Systemic disease (HIV)
-Malnutrition
Pre-existing gingivitis, poor oral hygiene, history of NPD
Psychological stress, lack of sleep
Smoking
54
Q

Histopath of NPD

A

Necrosis of epithelium and superficial layers of the connective tissue.
Hyperemic CT with engorged capillaries and dense infiltrations of PMNs.

Listgarten 1965:
Bacterial zone
Neutrophil rich zone
Necrotic zone
Spirochetal infiltration zone
55
Q

NPD: Clinical presentation

A

Ulceration and necrosis of interproximal papillae
Painful gingiva
Bleeding (spontaneous, on slight provocation)

56
Q

NPD:

Differential Diagnosis

A

Primary Herpetic Gingivostomatitis

Oral mucosal diseases

57
Q

NPD: Acute Treatment

A

Debridement
Oral rinses (0.12% CHX)
Antibiotics: metronidazole (250mg TID)

58
Q

Periodontal Abscesses

A

localized collection of pus
within the tissues of the periodontium.

3rd most Common emergency condition (8-14%)

59
Q

Gingival Abscess

A

Etiology: irritation from foreign bodies forcefully embedded into previously healthy tissues.
Localized, painful, rapidly expanding lesion with sudden onset.
Generally limited to the marginal gingiva or interdental papillae.

60
Q

Periodontal Abscess

A

A localized purulent inflammation in the periodontal tissues.
Often occur in molar sites.
Associated with preexisting periodontitis
Localization occurs when drainage through pocket is impaired.

61
Q

Periodontitis-related Abscess

A 
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
62
Q

Non-Periodontitis-related Abscess

A 
Foreign body impaction
Oral hygiene devices
Food particles
Root morphology alterations
Iatrogenic (endodontic perforation)
External root resorption
Cemental tears
63
Q

development of a periodontal abscess, the first step is

A

the bacterial invasion of the soft tissues surrounding the periodontal pocket, all periodntitis relted bacteria can be involved.
but P.g has been detected with high frequency in the periodontal abscess.
The invision of the bacteria attracts pmn to the site, which kill and encapsulate he bacteria.

64
Q

Periodontal Abscess Diagnosis

A 
Pain
Swelling
Redness
Suppuration
Spontaneous or occur after pressure
Gingival tenderness
Associated with deep pocket, BOP, mobility.
Radiographic: widened PDL, bone loss
Fever, malaise, lymphadenopathy
65
Q

Differential Diagnosis

A 
Periapical (endodontic) abscess
Vertical root fracture
Endo-perio abscess
Other
Osteomyelitis
Periodontal cyst
Manifestation of systemic diseases
66
Q

Periodontal Abscess - Therapy

A 
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
67
Q

Simplified Oral Hygiene Index (OHI-S)

purpose

A

To assess oral cleanlines by estimating the tooth surface covered with debris and/or calculus

68
Q

OHI-S: Components

A

Simplified Debris Index

Simplified Calculus Index

69
Q

OHI-S: Tooth selection

A

Facial surfaces of # 3, 8, 14, 24

Lingual surface of # 19, 30

70
Q

Plaque Index (PlI)

A

The PlI assesses the amount of plaque at the gingival margin, examining the same anatomical units as the GI
Plaque scores range from {0} to {3}
A probe is used to distinguish between scores {0} and {1}. Visible plaque is scored a {2} or a {3}
The Pl-I is computed for a tooth, subject, or population
It parallels the Gingival Index (GI) of Löe & Silness
First published by Silness & Löe (1964)

71
Q

Turesky Modification of Quigley-Hein Plaque Index

A

Score 0: No plaque
Score 1: Spots of plaque at cervical margin
Score 2: Thin, continuous band of plaque,
£1 mm wide, at cervical margin
Score 3: A plaque band >1 mm but <1/3 of crown height
Score 4: Plaque covering ³ 1/3 but < 2/3 of crown height
Score 5: Plaque covering ³ 2/3 of crown height

72
Q

Turesky Modification of Quigley-Hein Plaque Index

A

The Quigley-Hein index is biased toward the gingival third of the tooth surface
Facial and lingual surfaces are examined
Plaque is made visible using a disclosing agent and scored using a {0} to {5} scoring system
Scores are computed for subject, population
It is the most frequently used plaque index in clinical trials
Quigley & Hein (1962); Turesky et al. (1970)

73
Q

Calculus Indices

A 
Simplified Oral Hygiene Index (OHI-S)
Periodontal Disease Index (PDI)
Probe Method (Volpe-Manhold)
Calculus Surface (Severity) Index (CSI)
Marginal Line Calculus Index (MLCI)
NIDR Calculus Index
74
Q

NIDR Calculus Index

A

0 Calculus is absent
1 Supragingival calculus, but no subgingival calculus is present
2 Supragingival and subgingival, or subgingival calculus only is present

75
Q

Volpe-Manhold Index

A

Determines the quantity of supragingival calculus
Lingual surfaces of lower anteriors (#22-27)
Quantity is determined in mm of calculus along the 2 diagonal and the central lines drawn over the lingual surface of each tooth
Index, expressed in mm, is computed for tooth, subject, population
Most frequently used calculus index in longitudinal studies
Published by Volpe & Manhold (1962)

*High inter-examiner and intra-examiner reproductivity

Perio Exam 2 (20 decks)

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