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Perio E2 > Gingivitis > Flashcards

Gingivitis Flashcards

1
Q

Microbiological determinants of periodontal health

A

Supragingival plaque compostion

Subgingival biofilm compostion

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2
Q

Host determinants: Local

A

Periodontal pockets
Dental restorations
Root Anatomy
Tooth position and crowding

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3
Q

Host Determinants: Systemic (modifying factors)

A

Host immune function
Systemic health
Genetics

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4
Q

Predisposing Factors

A

Any Agent or condition that contributes to the accumulation of plaque

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5
Q

Modifying Factors

A

Any agent or condition that alters the way in which an individual responds to subgingival plaque accumulation

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6
Q

Plaque induced gingivitis is an inflammatory response to the gingival tissues resulting from

A

Bacterial plaqu accumulation located at and below the gingival margin

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7
Q

Plaque induced gingivitis is a loss of _________ between the biofilm and host immune response and _________

A

Symbiosis

Development of an incipient dysbisosis

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8
Q

Common clinical changes from health to gingivitis

A 
Color
Texture
Edema
Bleeding
Exudate
Plaque
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9
Q

Color changes in Gingiva

A

Normal=Coral pink
Inflamed =Red
(Increased vasculaziation and decreased epithelial keratinzation)
Severely red=Red and cyanotic
(Vascular proliferation and reduction in keratinization + venous stasis)

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10
Q

Gingival Bleeding

A

With increased inflammation dilation and engorgment of capilairtes or thinking of sulcular epithelium

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11
Q

Healthy Gingiva feels

A

Firm and resilient

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12
Q

With inflammation Gingiva consistency

A

Increase in Extracellular fluid and exudate

Degeneration of connective tissue and epithelium

Engorged connective tissue and thinning of epithelium

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13
Q

Chronic inflammation can induce

A

Fibrosis and epithelial proliferation

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14
Q

Gingiva necrosis

A

Sloughing with grayish flake like debris

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15
Q

Surface texture

A

Healthy-dull with stippling

Inflammation-loss of stippling smooth and shiny if exudate change occurs
Firm and Nodular if firbtocic changes occur

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16
Q

Shape of gingiva

A

Healthy-scalloped with filing interdental spaces

Inflammation-knife edge gingival adaptation or loose gingival margins
In some cases clefts or festoons may develop

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17
Q

Chronic inflammatory response characteristic with

A

Exudative and proliferative features

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18
Q

Clinically ___lesions with

A

Deep red lesions with soft friable smooth shiny surface and bleeding tendency

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19
Q

Clinical fibrotic will show as

A

Firm resilient and pink lesion with abundant fibroblasts and collagen fibers

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20
Q

Characteristics common to all dental plaque induce inflammatory gingival conditions

A

1 Sings and symptoms limited to gingiva
2 Reversibility of the disease by removing the etiology
3 The presence of high dental plaque
4 Systemic modifying factors which can alters the severity of inflammation
5 stable attachment levels

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21
Q

Systemic modifying factors

A 
Sex steroids
Hyperglycemia
Leukemia
Smoking 
Malnutrition
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22
Q

Oral factors enhancing plaque accumulation

A

Prominent subgingival restoration margins

Hyposalivation

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23
Q

Plaque induced gingivitis can be due to

A

Biofilm
Modifying factors
Drug induced gingival enlargements

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24
Q

Generalized

A

> 30% of the sites with glial signs of gingival inflammation

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25
Q

Incipient gingivitis

A

Only a few sites are affected with mild signs of gingival inflammation can be considered gingival health having high risk of developing gingivitis

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26
Q

Reduced periodontist

A

Following active periodontal treatment and the resolution of inflammation from periodontitis is a common finding

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27
Q

Plaque induced gingivitis on a reduce periodontist is characterized by

A

The return of bacterially induced inflammation to the gingival margin on a reduced periodontium with no evidence of progressive attachment loss

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28
Q

Primary etiologic factors =

A

Bacterial plaque

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29
Q

Secondary etiologic always factors =

A

Local factors

  • calculus
  • Marginal deficiencies
  • Malocculsion
  • Tooth/root anomalies
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30
Q

Periodontist starts with

A

Gingivitis

Gingivitis does not always progress into periodontitis

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31
Q

Plaque induced gingivitis does not directly cause

A

Tooth loss

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32
Q

Primary preventive strategy for periodontitis

A

Managing gingivitis

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33
Q

What is the most common for of periodontal disease

A

Plaque induced gingivitis

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34
Q

Supracrestal attached tissues

A

.69 mm sulcus depth
.97 epithelial attachment
1.07 connective tissue attachment

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35
Q

Supracrestal attached tissue minimum

A

3 mm coronal to alveolar crest

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36
Q

3 commonly used drug types that are associated with gingival enlargement

A

Anticonvulsants
Immunosuppressant
Calcium channel blocking agents

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37
Q

Genetic developmental Disorders

A

Hereditary gingival fibromatosis

-gingival enlargement

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38
Q

Hereditary gingival Fibromatosis

A

Diffuse gingival enlargement

May interfere with or prevent tooth eruption, malocclusion

May slow with age; require surgery

Can be a single diseae or a part of a syndrome

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39
Q

Hereditary gingival Fibromatosis possible mechanism

A

TGF-b1 favor the accumulation of ECM

May be located on chromosomes 2 in human

“Son of sevenless 1”

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40
Q

In. Hereditary gingival Fibromatosis the gingiva

A

Just keeps growing

Can grow so much start chewing on it

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41
Q

Bacterial origin

A

Necrotizing periodontal diseases

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42
Q

Necrotizing stomatitis

A

Ulceration extending from gingival margin including beyond the MGJ

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43
Q

NPD constant flora primarily contains

A

Treponema app
Selenomonas
Fusobacterium
Prevotella intermedia

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44
Q

NPD initial presentation

A

Very typical

Start at tip of papilla

White necrotic spot

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45
Q

Should gingivitis cause pain

A

No

NPD does
Burning

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46
Q

Gingival lesions of bacterial origin predisposing factors

A

Systemic diseases like ulcerative colitis blood discards
Abnormalities of WBC function
Patients suffering from AIDs

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47
Q

NPD may progress to

A

Cancrum oris

Noma

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48
Q

Primary hermetic gingivostomatis

A

herpes simplex virus

Not limited to gingiva

1-2 weeks

Contagious

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49
Q

NPD ulceration are

A

Yellowish white plaque

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50
Q

PHS ulceration

A

Multiple vesicles which burst leaving small round fibrin covered ulcers

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51
Q

Is NPD contagious

A

Nope

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52
Q

Coxsackie virus -hand foot and mouth disease

A

A common contagious vascular viral diseae affecting skin and oral mucosa including gingiva

Mostly children

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53
Q

herpes Simplex virus

A

Type 1 and 2

Varicella zoster virus

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54
Q

Herpes ________ usually causes oral manifestations

A

Simplex 1

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55
Q

Primary hermetic gingivostomatitis

A

Through oral musical epithelium virus penetrates a neural ending and travels tot eh trigeminal ganglion

56
Q

Primary hermetic gingivostomatitis symptoms

A

Painful severe gingivitis with redness
Ulceration Smith’s erofibrnous exudate
Edema accompanied by stomatitis

57
Q

Primary hermetic gingivostomatitis characteristics

A

Incubation period is one week
Formation of vesicles which rupee coalesce and leave fibrin coated ulcers
Healing within 10-14 days

58
Q

Recurrent intraoral herpes simplex lesions

A

Herpes virus can stay later in trigeminal ganglion for years

Found in gingivitis, NPD and periodontist

59
Q

More primary viral infections occur

A

At older ages in industrialized society

60
Q

Recurrent hermetic infection

A

Herpes labialis (more than once a year)

vermilion border and or skin adjacent to it

Trauma UV light fever menstariton

61
Q

Herpes Zoster

A

Unilateral lesion
Laten in DRG
2nd and 3rd branch of the trigeminal ganglion

Small ulcers usually on tongue palate and Gingiva

62
Q

Molluscum contagiosum virus

A

Poxvirus family
Contagious disease with infrequent oral manifestation
Infants with immature immune systems
In adults lesions in genital areas and often sexually transmitted

63
Q

Human Papilloma Virus

A

25 detected in oral lesions

More than 100 types

64
Q

HPV benign lesions

A

Squamous cell papilloma
Condylomata acuminatum
Verruca vulgaris
Focal epithelial hyperplasia

Asymptomatic

65
Q

Most common mouth mycosis

A

Candidosis

66
Q

Most common fungal infections that may affect oral cavity

A

Candidosis

Histoplasmosis

67
Q

C. Albicans

A

Normal commensal organism

Also opportunistic pathogen

68
Q

Candidosis

A

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

69
Q

Candidosis can be seen in

A 
Diabetes
Vaginal candidosis
Pregnancy
Contraceptives
Cancer
Antibiotic long term use
70
Q

Candidosis diagnosis

A

A culture of Nickerson medium at room temp

Microscopic examination of a smear fo the material scrapped from the lesion and stained

71
Q

Candidosis treatment

A

the use of antimycotic antifungal agents

72
Q

2 types of candidosis

A

Erthematous candidosis

Psedumebranous candidosis

73
Q

Pseudomembranous

A

whitish patches that can be wiped off

74
Q

Erythematous

A

Red assocaited wit pain

75
Q

Plaque type

A

White has plaque that cannot be removed need to be differentiated from oral leukoplakia

76
Q

Nodular

A

Slightly elevated nodules of white or reddish color

77
Q

Histoplasmosis

A

Granulomas our disease

Bird poop

78
Q

Histoplasmosis is usually secondary to

A

Lung issues

79
Q

Histoplasmosis in the oral cavity

A

Can be anywhere. Mostly on tongue

Nodular or papillary may become ulcerative

80
Q

Type I allergic reactions

A

Immediate type

Mediated by IgE

81
Q

Type IV reactions

A

Delayed

Mediated by T cells
12-48 hours following contact with allergen

**what we usually talk about

82
Q

Plasma Cell Gingivitis

A

Uncommon inflammatory condition
Usually anterior maxillary gingiva
Uncertain etiology

83
Q

Diffuse gingivitis

A

Due to contact allergy

84
Q

Erythema multiforme

A

Acute sometimes recurrent affecting both mucous and membranes and skin

Oral involvement is uncommon

Swollen lips with crust

Bullae that rupees and leaves extensive ulcers

85
Q

Erythema multiforme skin lesion

A

Iris appearance + bullae

86
Q

Erythema multiforme appears to be

A

A cytokines immune reaction towards keratinocytes precipitous by a wide range of factors include herpes simplex and various drugs

87
Q

Bulls

A

A large blister or skin vesicles filled with fluid

88
Q

Ulcerative

A

Affected with an ulcer open sore or lesion of the skin or muscle accompanied by sloughing of inflamed necrotic tissue

89
Q

Atrophy

A

A wasting a decreasing in size of tissue

90
Q

Plaque

A

A patch on the skin or on a mucous surface

91
Q

Reticular

A

Mesh in the form of network

92
Q

Papula

A

A small inflammatory congested spot on the skin a pimpl q

93
Q

Pemiphigus Vulagris

A

Formation of intraepitheali bullae in skin and mucous membranes

-Painful desquamtive lesions erosions or ulceration

94
Q

Pemiphigus Vulagris histology: Acantholyusis

A

Due to destruction of desmosomes pericellular perineal depsosts of IgG and C3

Circulating autoantibodies against interpetheial adhesion molecules

95
Q

Pemphigoid

A

A group of disorders in which autoantibodies towards components of the basement membranes results in detachment of the epithelium from the CT

96
Q

Pemphigoid histology

A

Autoantibody reactions against HEMIdesomomes and lamina Lucinda components

97
Q

Pemphigoid 3 types

A

Bulbous
Benign Mucous Membrane
Cicatricial (scar formation)

98
Q

Pemphigoid Nicholsky sign

A

Rubbing gingiva creates bulla formation

99
Q

Pemphigoid treatment

A

Plaque removal with daily use of chlorhexidine and topic corticosteroid

100
Q

Pemphigoid deposits of

A

C3
IgG
other Igs

101
Q

Lichen Planus

A

Oral involvement alone is common
Rare in children
Skin lesions (whickham striae)

Can turn into cancer

102
Q

Lichen planus clinical appearance

A 
Various clinical appearance 
Papular
Reticular
Plaque like
Strophic
UIlcerative
Bulbous
103
Q

Lichen Planus histochemistry sub-epithelial

A

Band like accumulation of lymphocytes and macrophages characteriesitic of type IV hypersensitivity reaction

104
Q

Lichen Planus histochemistry fibrin will be in

A

The basement membrane

Deposits of IgM C3,4,5

Inflammatory reaction toward an undifferentiated antigen in basal epithelial layer zone

105
Q

Lupus erythematosus

A

AI CT disorders in which autoantibodies form to various cellular constituents

106
Q

Lupus erythematosus central atrophic area

A

With small white dots surrounded by irradiating fine white striae with a periphery of telangiectasia

107
Q

Lupus erythematosus signs

A

Lesions can be ulceration and cannot be differentiated from leukoplakia or atrophied oral lichen planus

Together with butterfly skin rash

108
Q

Lupus erythematosus histology

A

Degeneration of basal cells and increased width of the basement membrane

Deposits of various Igs C3 and fibrin along the basement membrane

109
Q

Lupus erythematosus 2 forms

A

Discord mild chronic which affects skin and mucous membrane

Systemic form

110
Q

Granulomas our inflammatory conditions

A

Crohns
Sarcoidosis

Persistent enlargement of the soft tissues in the oral cavity as well as the facial region can occur concomitant with various systemic conditions

111
Q

Reactive Processes: Irritation fribomal/focal fibrous hyperplasia

A

A focal fibrous hyperplasia caused by irritation

Sessile well circumscribed smooth surfaced nodules

Cell poor hyperplasia collagenous tissue

May show hyperkeratinziation

The size varies from small to large tumorlike processes with a diameter of several cm

112
Q

Calcified Fibroblastic Granumola (reactive processes)

A

Often reddish and ulcerated reactive lesion

Fibrous proliferation in which bone or cementum like hard tissue is formed

Highly cell rich areas below ulcerated sited

113
Q

Pyogenic Granulomas

A

Ulcerated

Can occur during pregnancy

Reddish or blush; lonulate; sessile or pedunculated

Highly vascular

114
Q

Peripheral Giant Cell Granulomas

A

Anywhere on gingival mucosa

Most common reactive lesions of the oral cavity

Pedunculated, sessile, red or purple, ulcerated

115
Q

Peripheral Giant Cell Granulomas is a focal collection of

A

Multi nucleatum osteoclast like giant cells with a richly cellular and vascular storm separated by collagenous septa

116
Q

Leukoplakia

A

A white lesion of the oral mucosa

Lesions are generally asymptomatic and cannot be rubbed off

117
Q

20% of leukoplakia lesions demonstrate some degree of dysplasia or carcinoma upon biopsy thus leukoplakia can be considered

A

a premalignat condition

118
Q

Leukoplakia lesions occurs most often on

A

Buccal mucosa
Mandibular gingiva
Tongue
Floor of mouth

119
Q

Leukoplakia which type of lesion present a greater risk for malignant transformation?

A

Non-homogenous and larger

120
Q

Erythroplakia

A

The red counterpart of leukoplakia

Usually a higher premalignat potential

Very uncommon

121
Q

Squamous Cell Carcinoma

A

Mandible Premolar and molar regions

Common in edentulous areas mobility of adjacent teeth

122
Q

Leukemia

A

Acute and chronic leukemia based on clinal behavior and lymphocytic/lymphoblastic and myeloid depending on their histogenetic origin

Oral lesions occur in both but more common in acute form

Bacterial and viral and fungal infections including candidosis and herpes simplex infection may also be present

123
Q

Lymphoma

A

General term given to tumors of the lymphoid system

Most common hematologic malignancy

Hodgkin and non-Hodgkin

Oral Hodgkin is rare

124
Q

Lymphoma may oringate form

A

B and T lymphocyte cell lines

125
Q

Metastasis to the gingiva

A

The majority are intraoesseous

Soft tissues metastasis from lung cancer

Most of themetastsis cases are carcinoma and not sarcoma

126
Q

Vitamin c deficient is characterized by

A

Gingival bleeding and soreness

Depressed immune response

127
Q

Frictional keratosis

A

Limited physical trauma from brushing may result in gingival hyperkeratosis a white leukoplakia like lesion

128
Q

Tooth brushing induce gingival ulceration

A

Varies from superficial gingival laceration to major loss of tissue resulting in gingival recession

129
Q

Factitious injury

A

Usually seen in young patients

Unusual tissue damage in areas that can easily be reached by fingers and instruments

130
Q

Chemical insults

A

Surface etching by various chemical products with toxic properties

131
Q

Thermal injury

A

Minor burns from hot beverages

132
Q

Factors that may cause oral pigmentation

A 
Drugs
Heavy metals
Genetics
Endocrine disturbances
Syndromes
Post inflammatory reactions
133
Q

Physiological pigmentation is usually

A

Symmetric occuringon the gingiva buccal mucosa hard palate lips tongue

134
Q

Smokers Melanosis

A

Melanocytic pigmentation of the oral mucosa due to cigarette smoking

Mostly observed not eh mandibular anterior facial gingiva

135
Q

Drug Induced pigmentation

A

May be caused by accumulation of melanin despots drug or drug metabolites synthesis of pigments under the influence of a drudge or deposition of iron following damage to vessels

136
Q

Drugs that cause DIP

A

Antimalraial drugs

Long term use of minocycline

Perio E2 (9 decks)

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