• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/92

Click to flip

92 Cards in this Set

  • Front
  • Back
Components of Periodontium vs Attachment apparatus
Periodontium - Cementum, PDL, Alveolar bone, Gingiva, Alveolar mucosa

Attachment apparatus- Cementum, PDL, Alveolar Bone
Marginal gingiva & properties
Free unattached gingiva normally 1mm
Free gingival groove about 50%
Ideal & normal depth of gingival sulcus
0mm Germ free animals
Clinically healthy is 2mm on lingual & facial, 3mm interproximal. 1.8mm avg
Attached gingiva width & Least?
Maxillary anterior 3.5-4.5
Mandibular is 3.3-3.9

Least amt of attached gingiva on first premolar
Attached vs Keratinized gingiva
Attached gingiva is keratinized gingiva minus marginal gingiva
Mucogingival junction
Junction between keratinized gingiva & oral mucosa. On facial and lingual of mandibular but only facial of maxillary b/c of hard palate.
Shape of interdental gingiva & function of?
Pyramidal or col. Shape of col and interdental gingiva is function of contact point
Healthy embrasures
Gingival embrasure filled with gingiva in health.
Diastema
No interdental papilla. Gingiva firmly bound to interdental bone
Microscopic analysis of Attached gingiva vs mucosa
Attached gingiva is keratinized with rete pegs.

Mucosa has loose CT with more blood vessels. Thinner & no rete pegs
Color changes are only indicative of what?
Gingivitis and not PD
Pigmentation properties
Caused by melanin gives color to skin, gingiva, & oral mucosa

Not always in detectable quantities
Color a function of?
Vascular supply, keratinization, Thickness, pigmentation
Size a function of?
Vascular supply, cellular & intercellular elements
Contour a function of? & properties
Shape of teeth, alignment, contact, embrasures

Scalloped shaped, lingual is horizontal & thickened
Consistency/Tone of gingiva
Should be firm & resilient. Spongy is indicative of disease
Texture/stippling & factors for keratinization
Underlying connective tissue has factors to promote keratinization of gingiva

Free gingiva is smooth

Stippling found only on attached gingiva produced by protuberances and depressions in gingiva. Inflammation causes glossy surface & loss of stippling

May not be present, none at birth, increases, then decreases with age.
Position of gingiva?
During eruption margin & sulcus at tip of crown. Margin of free gingiva in mature tooth is at CEJ but can move coronal in hyperplasia & edema
2 types of eruption
Active - tooth move in direction of occlusal

Passive - Gingiva migrates apically to expose tooth
Anatomic vs clinical crown & root
Anatomic crown is covered with enamel & 1/3 is covered with gingiva. Clinical crown is only 2/3 anatomical.

Anatomic root is covered with cementum, clinical root is covered with periodontal tissues
As teeth go through attrition?
Active eruption keeps pace to maintain occlusion. Cementum is deposited at apices & root furcations. Bone also forms

Tooth lose by attrition is replaced by lengthening root & sulcus depth
Bleeding?
Indicative of gingivitis only.

Normal sulcus will not bleed when probed. Inflammation will have vasodilation & thus bleeding when probed.
Cells found in gingival epithelium
PMNs & Lymphocytes, Keratinocytes, melanocytes, langerhans cells, merkel cells
OGE properties
Cornified
extensive cell-cell Attachments
extensive Interdigitations
permeability Barrier
Stratified
Keratin filament assembly
Type I + Type II chain
Dimer
Tetramer
Protofilament
Keratin Filament
OSE properties & Cell layers
CAIBS opposite

Basal Layer - Flat cells
Inner Differentiation layer - Desmosomes
Outer Differentiation layer - Phagocytic & lysosomal activity

Presence of some PMNS and Lymphocytes is normal
JE properties
Develops from EO & Oral mucosa
Hemidesmosomes & Internal basal lamina attaches to tooth
Lysosomal & phagocytic
Permeability barrier not there
Transmigration of PMNs into sulcus
Internal basal lamina of JE (4)
Mineralization creates direct mineralized bond to enamel of dental cuticle

hemidesmosome attachments

Thick and multi-layered for strength

No collagen IV, only proteoglycans and laminin in IBL
Intraepithelial nerve endings
Found mostly where?
Does what?
Contains?
Highest in JE
C-fibers
Substance P, CGRP
Gingival Connective Tissue properties
Stomodeal mesenchyme development
Collagens 1,3,4,5,6,7
Highest collagen turnover
Cells of Gingival CT
Fibroblasts
Endothelial
Mast
Inflammatory - PMN, Lympho, Plasma
Macro
Adipocyte
Pericytes
Gingival Fibers
Gingivaldental
Circular
Semicircular
Transgingival
Transseptal
Blood supply to gingiva
PDL arterioles
Interdental arterioles
Supraperiosteal arterioles
Functions of PDL
Supportive
Sensory
Nutritive
Formative
Origin of fibroblasts
From neural crest
Fibers of PDL
Principal fibers
Indifferent fibers
Sharpey fibers
Oxytalan fibers
Principal fibers of PDL
Gingivodental
Alveolar crest
Transseptal
Interradicular
Horizontal
Oblique
Apical
PDL characteristics
.25mm wide
.39mm widest at crest
Load inc density
Age dec density
60% dense 40% loose CT around neurovascular bundle
PDL compartments
Bone compartment - rich in cells & blood vessels
Middle zone - less cells & thin collagen
Cementum - Dense collagen, avascular
Components of alveolar bone
Cortical plate - compact bone with haversian systems

Alveolar Bone proper - Cribriform plate & Lamina dura

Interdental septum - Cancellous bone
Alveolar bone defects causes & types
Prominent root contour
Malposition
thin facial cortical plate

Dehiscence - includes marginal bone

Fenestration - Marginal bone intact
Cornelius Celsus
4 cardinal signs of inflammation

Rubor Tumor Calor Dolor
Gingivitis Types & Pain
Acute
Subacute
Recurrent
Chronic

Painful in acute
Chronic usually painless
Etiology Def & of gingivitis
The study of causes of disease

Biofilm(Plaque) + Host Response = Gingivitis
Colors in gingivitis types
Acute is bright red, erythematous

Chronic is shades of red & blue from marginal gingiva to attached gingiva
Factors contributing to gingival overgrowth
Genetic - Hereditary ging fibromatosis
Developmental - Altered passive eruption
Medication
Plaque induced
Texture of gingiva during chronic gingivitis
Gingiva becomes smooth & shiny
Gingival recession etiology (7)
Gingival Abrasion
Tooth malposition
Occlusal trauma
Ablation
High Frenum
Inflammation
2 earliest signs of gingival inflammation preceding gingivitis
Increased production of gingival fluid

Bleeding upon probing
Systemic disturbances causing spontaneous gingival bleeding (5)
Pregnancy
Anticoagulants
Platelet disorder
Coagulation disorder
Vascular abnormalities
Fibrotic gingiva Cause & symptoms
Caused by chronic gingivitis
Firm & leathery appearance
Bleeding Increased sulcus depth
Pathways of Inflammation 5
Facial/lingual
Interproximal
Gingiva to Bone
Bone to PDL
Gingiva to PDl
Periodontal pocket circle
Plaque, inflammation, pocket formation, more plaque
Contents of pocket
Bacteria
Bacterial products
Food debris
PMNLs
Desquamated Epithelial cells
Purulent exudate
GCF
Plaque covered calculus
Ways to deepen gingival sulcus
Coronal movement of gingival margin
Apical migration of attachment
Combination
Types of pockets
Gingival = Pseudopocket
Periodontal = True
Suprabony - Base of pocket coronal to bone, Horizontal bone loss, Transseptal fibers restored horizontally, PDL horizontal & oblique

Infrabony - Base of pocket below bone, Angular bone loss, Transseptal fibers restored obliquely, PDL follows angular pattern
Limitations of Radiographs
Distortions
Can't see facial/lingual bone
Do not reveal minor destructive changes
Changes in angulation
Purulent Exudate (3)
Does not indicate pocket depth of severity
Can be seen in both deep and shallow pockets
Not necessarily present in deep pockets
Tooth position is maintained by
Normal periodontium
Forces - occlusal, lips, cheek
Pathological tooth migration etiology
Bone Loss
Forces from tongue, lips, cheek
Pressure from fluid in pocket
Eruption Forces
Oral habits
Tooth mobility classification
0 - no movement
1 - slight movement
2 - Facial lingual movement <1mm
3 - Facial lingual movement >1mm as well as apical movement
Increased mobility can be caused by
Bone loss
Pregnancy, hormonal changes
Occlusal trauma
periodontal surgery
Extention of inflammation of periapical abcess
When there is no attachment loss
Quiescence or Remission
Exacerbation of Active Disease
When there are periods of attachment loss alternating with periods of remission
Site Specificity & changes?
Not all sites are involved

Severity can be increased by Further breakdown of existing sites & new sites breaking down
Gingivitis Stage 1 (4)
Vascular dilation
Increased blood flow
Migrations of PMNs into JE & lamina propria
Increased GCF
Gingivitis Stage 2 (6)
Proliferation of blood vessels
Increased lymphocytes (Tcells)
Rete pegs in JE
Bleeding upon probing
Collagen degradation
Cytotoxic effects on fibroblasts
Role of PMNs & Macrophages
Both:
Clears bacteria & products
Can damage tissues by leaking MMPs & ROS from PMNs

Macro:
Antigen presentation
Phagocytose apoptotic & necrotic cells
Secretion of complement proteins
Gingivitis Stage 3 (6)
Increased rete pegs
Increased collagen destruction
Plasma cells
More PMNs
Congested venules - stasis
Changes in color & texture of gingiva
Role of T cells (3)
Secrets Interleukins
T helper cell aids in B cell differentiation
No evidence of CD8 T cell in periodontal lesion
Plasma Cells
Secrets IgG, IgA, IgM to direct against specific antigens. Also has some polyclonal response to superantigens.
Non specific T cell activation
PAMPs recognized by PRRs & Toll like receptors

Superantigens can bind to MHCII &
T cell independent B cell activation
Some large polysaccharides ex. on flagella have many repeating epitopes that can activate B cells independent of T cells.

IgM class with lower affinity & promotes phagocytosis
Gingivitis Stage 4
Same histopathology as stage 3 plus bone absorption
Beginning of periodontal breakdown
B cell Leision
Episodic nature of periodontal disease
Tissue destruction occurs in episodic acute inflammation. Followed by longer periods of inactivity where fibrosis can occur
Bacterial mechanisms for tissue damage
Secrete toxins
Shed LPS
Activate MMPs
Activate cytokines
Induce apoptosis
Express proteases
Role of Prostaglandins in periodontal disease
Suppression of fibroblast proliferation & collagen synthesis

Stimulates osteoclastic bone resorption
NUG Symptoms & microbes involved
Painful necrosis of interdental tissue, fetid breath, pseudomembrane formation

Invasion by spirochetes, prevotella intermedia & fusobacterium nucleatum
Steroid Hormone influenced gingivitis
Intense inflammation, edema & enlargement of gingiva

Associated with pregnancy puberty, menstrual cycle, etc

Can progress to pyogenic granuloma

Characterized by exaggerated response to plaque
Medication induced gingival overgrowth
Phenytoin, cyclosporin, calcium channel blockers

Painless beadlike enlargement of facial and lingual gingival margin & interdental papillae
Desquamative gingival leisions
Sloughing of gingival epithelium

Many are oral manifestations of systemic diseases

Erosive lichen planus
Benign mucous membrane pemphigoid
bullous pemphigoid
Pemphigus vulgaris
Pemphigus
Intraepithelial clefting above basal layer
Intracellular antibodies
Acantholysis is present
Pemphigoid
Subepithelial clefting with an intact basal layer from basal lamina
Antibodies in basal membrane
Frequently found in chronic periodontitis
Subgingival calculus
Chronic periodontitis associations
Diabetes mellitus, HIV
Local factors
Environmental factors such as smoking & emotional stress
Chronic periodontitis classifications
Extent
Localized vs Generalized 30% threshold

Severity
Slight 1-2mm attachment loss
Moderate 3-4mm
Severe >5mm
Aggresive periodontitis Characteristics
Infected with Actinobacillus actinomycetemcomitans

Abnormalities in phagocyte function

Hyperreactive Macrophages to produce IL1 & PGE
Aggresive Periodontitis Forms
Localized:
- Circumpubertal onset
- First molar or incisor with proximal attachment loss on atleast 2 permanent teeth, atleast 1 first molar
- robust serum antibody response

Generalized
- Onset before 30
- Atleast 3 permanent teeth excluding first molars or incisors
-Pronounced episodic destruction of periodontium
- Poor serum antibody response
Periodontitis associated with systemic diseases
HIV
Diabetes Mellitus
Downs syndrome
Neutropenias
HIV & periodontitis
Linear gingival erythema
Necrotizing uncerative periodontitis
NUP pathology & systemic causes
Necrosis of gingival tissues, PDL, & bone

HIV
Immunosuppression
Severe malnutrition
Refractory disease
Disease in multiple sites where there is continued attachment loss after appropriate therapy