Gingivitis Flashcards
1
Q
Microbiological determinants of periodontal health
A
Supragingival plaque compostion
Subgingival biofilm compostion
2
Q
Host determinants: Local
A
Periodontal pockets
Dental restorations
Root Anatomy
Tooth position and crowding
3
Q
Host Determinants: Systemic (modifying factors)
A
Host immune function
Systemic health
Genetics
4
Q
Predisposing Factors
A
Any Agent or condition that contributes to the accumulation of plaque
5
Q
Modifying Factors
A
Any agent or condition that alters the way in which an individual responds to subgingival plaque accumulation
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
7
Q
Plaque induced gingivitis is a loss of _________ between the biofilm and host immune response and _________
A
Symbiosis
Development of an incipient dysbisosis
8
Q
Common clinical changes from health to gingivitis
A
Color Texture Edema Bleeding Exudate Plaque
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)
10
Q
Gingival Bleeding
A
With increased inflammation dilation and engorgment of capilairtes or thinking of sulcular epithelium
11
Q
Healthy Gingiva feels
A
Firm and resilient
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
13
Q
Chronic inflammation can induce
A
Fibrosis and epithelial proliferation
14
Q
Gingiva necrosis
A
Sloughing with grayish flake like debris
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
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
17
Q
Chronic inflammatory response characteristic with
A
Exudative and proliferative features
18
Q
Clinically ___lesions with
A
Deep red lesions with soft friable smooth shiny surface and bleeding tendency
19
Q
Clinical fibrotic will show as
A
Firm resilient and pink lesion with abundant fibroblasts and collagen fibers
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
21
Q
Systemic modifying factors
A
Sex steroids Hyperglycemia Leukemia Smoking Malnutrition
22
Q
Oral factors enhancing plaque accumulation
A
Prominent subgingival restoration margins
Hyposalivation
23
Q
Plaque induced gingivitis can be due to
A
Biofilm
Modifying factors
Drug induced gingival enlargements
24
Q
Generalized
A
> 30% of the sites with glial signs of gingival inflammation
25
Incipient gingivitis
Only a few sites are affected with mild signs of gingival inflammation can be considered gingival health having high risk of developing gingivitis
26
Reduced periodontist
Following active periodontal treatment and the resolution of inflammation from periodontitis is a common finding
27
Plaque induced gingivitis on a reduce periodontist is characterized by
The return of bacterially induced inflammation to the gingival margin on a reduced periodontium with no evidence of progressive attachment loss
28
Primary etiologic factors =
Bacterial plaque
29
Secondary etiologic always factors =
Local factors
- calculus
- Marginal deficiencies
- Malocculsion
- Tooth/root anomalies
30
Periodontist starts with
Gingivitis
Gingivitis does not always progress into periodontitis
31
Plaque induced gingivitis does not directly cause
Tooth loss
32
Primary preventive strategy for periodontitis
Managing gingivitis
33
What is the most common for of periodontal disease
Plaque induced gingivitis
34
Supracrestal attached tissues
.69 mm sulcus depth
.97 epithelial attachment
1.07 connective tissue attachment
35
Supracrestal attached tissue minimum
3 mm coronal to alveolar crest
36
3 commonly used drug types that are associated with gingival enlargement
Anticonvulsants
Immunosuppressant
Calcium channel blocking agents
37
Genetic developmental Disorders
Hereditary gingival fibromatosis
| -gingival enlargement
38
Hereditary gingival Fibromatosis
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
39
Hereditary gingival Fibromatosis possible mechanism
TGF-b1 favor the accumulation of ECM
May be located on chromosomes 2 in human
“Son of sevenless 1”
40
In. Hereditary gingival Fibromatosis the gingiva
Just keeps growing
Can grow so much start chewing on it
41
Bacterial origin
Necrotizing periodontal diseases
42
Necrotizing stomatitis
Ulceration extending from gingival margin including beyond the MGJ
43
NPD constant flora primarily contains
Treponema app
Selenomonas
Fusobacterium
Prevotella intermedia
44
NPD initial presentation
Very typical
Start at tip of papilla
White necrotic spot
45
Should gingivitis cause pain
No
NPD does
Burning
46
Gingival lesions of bacterial origin predisposing factors
Systemic diseases like ulcerative colitis blood discards
Abnormalities of WBC function
Patients suffering from AIDs
47
NPD may progress to
Cancrum oris
Noma
48
Primary hermetic gingivostomatis
herpes simplex virus
Not limited to gingiva
1-2 weeks
Contagious
49
NPD ulceration are
Yellowish white plaque
50
PHS ulceration
Multiple vesicles which burst leaving small round fibrin covered ulcers
51
Is NPD contagious
Nope
52
Coxsackie virus -hand foot and mouth disease
A common contagious vascular viral diseae affecting skin and oral mucosa including gingiva
Mostly children
53
herpes Simplex virus
Type 1 and 2
| Varicella zoster virus
54
Herpes ________ usually causes oral manifestations
Simplex 1
55
Primary hermetic gingivostomatitis
Through oral musical epithelium virus penetrates a neural ending and travels tot eh trigeminal ganglion
56
Primary hermetic gingivostomatitis symptoms
Painful severe gingivitis with redness
Ulceration Smith’s erofibrnous exudate
Edema accompanied by stomatitis
57
Primary hermetic gingivostomatitis characteristics
Incubation period is one week
Formation of vesicles which rupee coalesce and leave fibrin coated ulcers
Healing within 10-14 days
58
Recurrent intraoral herpes simplex lesions
Herpes virus can stay later in trigeminal ganglion for years
Found in gingivitis, NPD and periodontist
59
More primary viral infections occur
At older ages in industrialized society
60
Recurrent hermetic infection
Herpes labialis (more than once a year)
vermilion border and or skin adjacent to it
Trauma UV light fever menstariton
61
Herpes Zoster
Unilateral lesion
Laten in DRG
2nd and 3rd branch of the trigeminal ganglion
Small ulcers usually on tongue palate and Gingiva
62
Molluscum contagiosum virus
Poxvirus family
Contagious disease with infrequent oral manifestation
Infants with immature immune systems
In adults lesions in genital areas and often sexually transmitted
63
Human Papilloma Virus
25 detected in oral lesions
| More than 100 types
64
HPV benign lesions
Squamous cell papilloma
Condylomata acuminatum
Verruca vulgaris
Focal epithelial hyperplasia
Asymptomatic
65
Most common mouth mycosis
Candidosis
66
Most common fungal infections that may affect oral cavity
Candidosis
| Histoplasmosis
67
C. Albicans
Normal commensal organism
Also opportunistic pathogen
68
Candidosis
Painless or slightly sensitive
Red and white lesions
Lesions can be scraped or separated from mucosa
69
Candidosis can be seen in
```
Diabetes
Vaginal candidosis
Pregnancy
Contraceptives
Cancer
Antibiotic long term use
```
70
Candidosis diagnosis
A culture of Nickerson medium at room temp
| Microscopic examination of a smear fo the material scrapped from the lesion and stained
71
Candidosis treatment
the use of antimycotic antifungal agents
72
2 types of candidosis
Erthematous candidosis
| Psedumebranous candidosis
73
Pseudomembranous
whitish patches that can be wiped off
74
Erythematous
Red assocaited wit pain
75
Plaque type
White has plaque that cannot be removed need to be differentiated from oral leukoplakia
76
Nodular
Slightly elevated nodules of white or reddish color
77
Histoplasmosis
Granulomas our disease
Bird poop
78
Histoplasmosis is usually secondary to
Lung issues
79
Histoplasmosis in the oral cavity
Can be anywhere. Mostly on tongue
Nodular or papillary may become ulcerative
80
Type I allergic reactions
Immediate type
Mediated by IgE
81
Type IV reactions
Delayed
Mediated by T cells
12-48 hours following contact with allergen
**what we usually talk about
82
Plasma Cell Gingivitis
Uncommon inflammatory condition
Usually anterior maxillary gingiva
Uncertain etiology
83
Diffuse gingivitis
Due to contact allergy
84
Erythema multiforme
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
Erythema multiforme skin lesion
Iris appearance + bullae
86
Erythema multiforme appears to be
A cytokines immune reaction towards keratinocytes precipitous by a wide range of factors include herpes simplex and various drugs
87
Bulls
A large blister or skin vesicles filled with fluid
88
Ulcerative
Affected with an ulcer open sore or lesion of the skin or muscle accompanied by sloughing of inflamed necrotic tissue
89
Atrophy
A wasting a decreasing in size of tissue
90
Plaque
A patch on the skin or on a mucous surface
91
Reticular
Mesh in the form of network
92
Papula
A small inflammatory congested spot on the skin a pimpl q
93
Pemiphigus Vulagris
Formation of intraepitheali bullae in skin and mucous membranes
-Painful desquamtive lesions erosions or ulceration
94
Pemiphigus Vulagris histology: Acantholyusis
Due to destruction of desmosomes pericellular perineal depsosts of IgG and C3
Circulating autoantibodies against interpetheial adhesion molecules
95
Pemphigoid
A group of disorders in which autoantibodies towards components of the basement membranes results in detachment of the epithelium from the CT
96
Pemphigoid histology
Autoantibody reactions against HEMIdesomomes and lamina Lucinda components
97
Pemphigoid 3 types
Bulbous
Benign Mucous Membrane
Cicatricial (scar formation)
98
Pemphigoid Nicholsky sign
Rubbing gingiva creates bulla formation
99
Pemphigoid treatment
Plaque removal with daily use of chlorhexidine and topic corticosteroid
100
Pemphigoid deposits of
C3
IgG
other Igs
101
Lichen Planus
Oral involvement alone is common
Rare in children
Skin lesions (whickham striae)
Can turn into cancer
102
Lichen planus clinical appearance
```
Various clinical appearance
Papular
Reticular
Plaque like
Strophic
UIlcerative
Bulbous
```
103
Lichen Planus histochemistry sub-epithelial
Band like accumulation of lymphocytes and macrophages characteriesitic of type IV hypersensitivity reaction
104
Lichen Planus histochemistry fibrin will be in
The basement membrane
Deposits of IgM C3,4,5
Inflammatory reaction toward an undifferentiated antigen in basal epithelial layer zone
105
Lupus erythematosus
AI CT disorders in which autoantibodies form to various cellular constituents
106
Lupus erythematosus central atrophic area
With small white dots surrounded by irradiating fine white striae with a periphery of telangiectasia
107
Lupus erythematosus signs
Lesions can be ulceration and cannot be differentiated from leukoplakia or atrophied oral lichen planus
Together with butterfly skin rash
108
Lupus erythematosus histology
Degeneration of basal cells and increased width of the basement membrane
Deposits of various Igs C3 and fibrin along the basement membrane
109
Lupus erythematosus 2 forms
Discord mild chronic which affects skin and mucous membrane
Systemic form
110
Granulomas our inflammatory conditions
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
Reactive Processes: Irritation fribomal/focal fibrous hyperplasia
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
Calcified Fibroblastic Granumola (reactive processes)
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
Pyogenic Granulomas
Ulcerated
Can occur during pregnancy
Reddish or blush; lonulate; sessile or pedunculated
Highly vascular
114
Peripheral Giant Cell Granulomas
Anywhere on gingival mucosa
Most common reactive lesions of the oral cavity
Pedunculated, sessile, red or purple, ulcerated
115
Peripheral Giant Cell Granulomas is a focal collection of
Multi nucleatum osteoclast like giant cells with a richly cellular and vascular storm separated by collagenous septa
116
Leukoplakia
A white lesion of the oral mucosa
Lesions are generally asymptomatic and cannot be rubbed off
117
20% of leukoplakia lesions demonstrate some degree of dysplasia or carcinoma upon biopsy thus leukoplakia can be considered
a premalignat condition
118
Leukoplakia lesions occurs most often on
Buccal mucosa
Mandibular gingiva
Tongue
Floor of mouth
119
Leukoplakia which type of lesion present a greater risk for malignant transformation?
Non-homogenous and larger
120
Erythroplakia
The red counterpart of leukoplakia
Usually a higher premalignat potential
Very uncommon
121
Squamous Cell Carcinoma
Mandible Premolar and molar regions
Common in edentulous areas mobility of adjacent teeth
122
Leukemia
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
Lymphoma
General term given to tumors of the lymphoid system
Most common hematologic malignancy
Hodgkin and non-Hodgkin
Oral Hodgkin is rare
124
Lymphoma may oringate form
B and T lymphocyte cell lines
125
Metastasis to the gingiva
The majority are intraoesseous
Soft tissues metastasis from lung cancer
Most of themetastsis cases are carcinoma and not sarcoma
126
Vitamin c deficient is characterized by
Gingival bleeding and soreness
Depressed immune response
127
Frictional keratosis
Limited physical trauma from brushing may result in gingival hyperkeratosis a white leukoplakia like lesion
128
Tooth brushing induce gingival ulceration
Varies from superficial gingival laceration to major loss of tissue resulting in gingival recession
129
Factitious injury
Usually seen in young patients
Unusual tissue damage in areas that can easily be reached by fingers and instruments
130
Chemical insults
Surface etching by various chemical products with toxic properties
131
Thermal injury
Minor burns from hot beverages
132
Factors that may cause oral pigmentation
```
Drugs
Heavy metals
Genetics
Endocrine disturbances
Syndromes
Post inflammatory reactions
```
133
Physiological pigmentation is usually
Symmetric occuringon the gingiva buccal mucosa hard palate lips tongue
134
Smokers Melanosis
Melanocytic pigmentation of the oral mucosa due to cigarette smoking
Mostly observed not eh mandibular anterior facial gingiva
135
Drug Induced pigmentation
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
Drugs that cause DIP
Antimalraial drugs
Long term use of minocycline
