Perio Yr1

Periodontium - Cementum, PDL, Alveolar bone, Gingiva, Alveolar mucosa

Attachment apparatus- Cementum, PDL, Alveolar Bone

Free unattached gingiva normally 1mm
Free gingival groove about 50%

0mm Germ free animals
Clinically healthy is 2mm on lingual & facial, 3mm interproximal. 1.8mm avg

Maxillary anterior 3.5-4.5
Mandibular is 3.3-3.9

Least amt of attached gingiva on first premolar

Attached gingiva is keratinized gingiva minus marginal gingiva

Junction between keratinized gingiva & oral mucosa. On facial and lingual of mandibular but only facial of maxillary b/c of hard palate.

Pyramidal or col. Shape of col and interdental gingiva is function of contact point

Gingival embrasure filled with gingiva in health.

No interdental papilla. Gingiva firmly bound to interdental bone

Attached gingiva is keratinized with rete pegs.

Mucosa has loose CT with more blood vessels. Thinner & no rete pegs

Gingivitis and not PD

Caused by melanin gives color to skin, gingiva, & oral mucosa

Not always in detectable quantities

Vascular supply, keratinization, Thickness, pigmentation

Vascular supply, cellular & intercellular elements

Shape of teeth, alignment, contact, embrasures

Scalloped shaped, lingual is horizontal & thickened

Should be firm & resilient. Spongy is indicative of disease

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.

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

Active - tooth move in direction of occlusal

Passive - Gingiva migrates apically to expose tooth

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

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

Indicative of gingivitis only.

Normal sulcus will not bleed when probed. Inflammation will have vasodilation & thus bleeding when probed.

PMNs & Lymphocytes, Keratinocytes, melanocytes, langerhans cells, merkel cells

Cornified
extensive cell-cell Attachments
extensive Interdigitations
permeability Barrier
Stratified

Type I + Type II chain
Dimer
Tetramer
Protofilament
Keratin Filament

CAIBS opposite

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

Presence of some PMNS and Lymphocytes is normal

Develops from EO & Oral mucosa
Hemidesmosomes & Internal basal lamina attaches to tooth
Lysosomal & phagocytic
Permeability barrier not there
Transmigration of PMNs into sulcus

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

Highest in JE
C-fibers
Substance P, CGRP

Stomodeal mesenchyme development
Collagens 1,3,4,5,6,7
Highest collagen turnover

Fibroblasts
Endothelial
Mast
Inflammatory - PMN, Lympho, Plasma
Macro
Adipocyte
Pericytes

Gingivaldental
Circular
Semicircular
Transgingival
Transseptal

PDL arterioles
Interdental arterioles
Supraperiosteal arterioles

Supportive
Sensory
Nutritive
Formative

From neural crest

Principal fibers
Indifferent fibers
Sharpey fibers
Oxytalan fibers

Gingivodental
Alveolar crest
Transseptal
Interradicular
Horizontal
Oblique
Apical

.25mm wide
.39mm widest at crest
Load inc density
Age dec density
60% dense 40% loose CT around neurovascular bundle

Bone compartment - rich in cells & blood vessels
Middle zone - less cells & thin collagen
Cementum - Dense collagen, avascular

Cortical plate - compact bone with haversian systems

Alveolar Bone proper - Cribriform plate & Lamina dura

Interdental septum - Cancellous bone

Prominent root contour
Malposition
thin facial cortical plate

Dehiscence - includes marginal bone

Fenestration - Marginal bone intact

4 cardinal signs of inflammation

Rubor Tumor Calor Dolor

Acute
Subacute
Recurrent
Chronic

Painful in acute
Chronic usually painless

The study of causes of disease

Biofilm(Plaque) + Host Response = Gingivitis

Acute is bright red, erythematous

Chronic is shades of red & blue from marginal gingiva to attached gingiva

Genetic - Hereditary ging fibromatosis
Developmental - Altered passive eruption
Medication
Plaque induced

Gingiva becomes smooth & shiny

Gingival Abrasion
Tooth malposition
Occlusal trauma
Ablation
High Frenum
Inflammation

Increased production of gingival fluid

Bleeding upon probing

Pregnancy
Anticoagulants
Platelet disorder
Coagulation disorder
Vascular abnormalities

Caused by chronic gingivitis
Firm & leathery appearance
Bleeding Increased sulcus depth

Facial/lingual
Interproximal
Gingiva to Bone
Bone to PDL
Gingiva to PDl

Plaque, inflammation, pocket formation, more plaque

Bacteria
Bacterial products
Food debris
PMNLs
Desquamated Epithelial cells
Purulent exudate
GCF
Plaque covered calculus

Coronal movement of gingival margin
Apical migration of attachment
Combination

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

Distortions
Can't see facial/lingual bone
Do not reveal minor destructive changes
Changes in angulation

Does not indicate pocket depth of severity
Can be seen in both deep and shallow pockets
Not necessarily present in deep pockets

Normal periodontium
Forces - occlusal, lips, cheek

Bone Loss
Forces from tongue, lips, cheek
Pressure from fluid in pocket
Eruption Forces
Oral habits

0 - no movement
1 - slight movement
2 - Facial lingual movement <1mm
3 - Facial lingual movement >1mm as well as apical movement

Bone loss
Pregnancy, hormonal changes
Occlusal trauma
periodontal surgery
Extention of inflammation of periapical abcess

Quiescence or Remission

When there are periods of attachment loss alternating with periods of remission

Not all sites are involved

Severity can be increased by Further breakdown of existing sites & new sites breaking down

Vascular dilation
Increased blood flow
Migrations of PMNs into JE & lamina propria
Increased GCF

Proliferation of blood vessels
Increased lymphocytes (Tcells)
Rete pegs in JE
Bleeding upon probing
Collagen degradation
Cytotoxic effects on fibroblasts

Both:
Clears bacteria & products
Can damage tissues by leaking MMPs & ROS from PMNs

Macro:
Antigen presentation
Phagocytose apoptotic & necrotic cells
Secretion of complement proteins

Increased rete pegs
Increased collagen destruction
Plasma cells
More PMNs
Congested venules - stasis
Changes in color & texture of gingiva

Secrets Interleukins
T helper cell aids in B cell differentiation
No evidence of CD8 T cell in periodontal lesion

Secrets IgG, IgA, IgM to direct against specific antigens. Also has some polyclonal response to superantigens.

PAMPs recognized by PRRs & Toll like receptors

Superantigens can bind to MHCII &

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

Same histopathology as stage 3 plus bone absorption
Beginning of periodontal breakdown
B cell Leision

Tissue destruction occurs in episodic acute inflammation. Followed by longer periods of inactivity where fibrosis can occur

Secrete toxins
Shed LPS
Activate MMPs
Activate cytokines
Induce apoptosis
Express proteases

Suppression of fibroblast proliferation & collagen synthesis

Stimulates osteoclastic bone resorption

Painful necrosis of interdental tissue, fetid breath, pseudomembrane formation

Invasion by spirochetes, prevotella intermedia & fusobacterium nucleatum

Intense inflammation, edema & enlargement of gingiva

Associated with pregnancy puberty, menstrual cycle, etc

Can progress to pyogenic granuloma

Characterized by exaggerated response to plaque

Phenytoin, cyclosporin, calcium channel blockers

Painless beadlike enlargement of facial and lingual gingival margin & interdental papillae

Sloughing of gingival epithelium

Many are oral manifestations of systemic diseases

Erosive lichen planus
Benign mucous membrane pemphigoid
bullous pemphigoid
Pemphigus vulgaris

Intraepithelial clefting above basal layer
Intracellular antibodies
Acantholysis is present

Subepithelial clefting with an intact basal layer from basal lamina
Antibodies in basal membrane

Subgingival calculus

Diabetes mellitus, HIV
Local factors
Environmental factors such as smoking & emotional stress

Extent
Localized vs Generalized 30% threshold

Severity
Slight 1-2mm attachment loss
Moderate 3-4mm
Severe >5mm

Infected with Actinobacillus actinomycetemcomitans

Abnormalities in phagocyte function

Hyperreactive Macrophages to produce IL1 & PGE

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

HIV
Diabetes Mellitus
Downs syndrome
Neutropenias

Linear gingival erythema
Necrotizing uncerative periodontitis

Necrosis of gingival tissues, PDL, & bone

HIV
Immunosuppression
Severe malnutrition

Disease in multiple sites where there is continued attachment loss after appropriate therapy