-
1,2,3-wall losses to the distal/mesial of a tooth (the 4th wall is the tooth itself); only refer to interproximal bone loss
-
when talking about buccal/lingual surfaces - reverse architecture/inconsistent margin
-
4-wall defect: only when the tooth extracted or osteotomy for implant or a large nutrient canal
-
"0-wall defect": horizontal bone loss
-
2-wall defect w/o interproximal bone, only lingual and buccal walls: crater
-
circumferencial defect: "4 wall defect" (4 one-wall defect)
-
In normal teeth, Bone is usually _______ to the CEJ – ______.
Bone that covers the root is _____ bone; Bone between teeth is _______ bone, which in normal environment is always more ________ – _______ architecture – bone follows contours of ___.
- 2mm apical
- parabolic form
- radicular
- interproximal
- coronal
- normal/positive
- CEJ
-
Horizontal bone loss results in _____ pocket, where the base of pocket is ______ to the crest of bone; vertical bone loss results in ______ pocket.
- suprabony
- coronal
- infrabony
-
probe to find out
- the attachment loss
- existence of disease activity – bleeding on probing
- how the bone is lost – determine the defect type
-
Periodontal disease results from a complex interplay between _______ and ________.
- subgingival biofilm
- the host immune-inflammatory response
-
Innate Immunity against periodontal disease
- intact epithelial barrier (junctional and sulcular epithelium)
- Outflow of Gingival Crevicular Fluid (GCF) from the sulcus - dilution and flushing
- neutrophil & macrophage in the sulcus - phagocytosis
- Antibodies in the GCF
-
Microbial Virulence Factors
- Lipopolysaccharide
- Bacterial Enzymes
- Microbial Invasion
- Initiate inflammatory response
- Contribute directly to tissue damage by release of noxious substances
-
Host-Derived Inflammatory Mediators
- Cytokines
- Prostaglandins
- Matrix Metalloproteinases (MMPs)
- Host response mainly protective
- Mainly responsible for tissue damage in periodontal disease
-
Increase in plaque + Host response = INFLAMMATION
-
Junctional Epithelium
- Non-keratinized
- Attached to tooth via hemidesmosomes
- Greater intercellular spaces—”Leaky”
- 1. Allows migration of Neutrophils and macrophages from connective tissue to sulcus
- 2. Ingress of bacterial products and antigens
-
GCF
originates from _________
has a flushing action in the ______
brings ______ of the host defense into the _________
flow _____ in inflammation (edema/swelling)
_______ are an important component
- postcapillary venules
- gingival crevice
- blood components
- sulcus
- increases
- Neutrophils
-
Saliva
____ attachment of bacteria to teeth and oral mucosa
_____ virulence factors, bacterial cell growth
___ antibodies to periodontal pathogens
-
Neutrophil - functions
- Feature of healthy gingiva
- barrier between subgingival plaque and gingival tissue
- “Professional” phagocytes
- Migrate from gingival plexus to CT in response to chemotactic gradient (pathway to bacteria)
- Secrete enzymes that cause degradation of junctional epithelium basement membrane and breaks down bacterial cell wall
-
Neutrophil Migration
1. Margination - injury slows down blood flow, neutrophils move to __________.
2. Adhesion - neutrophils attach to adhesion molecules (_______) within _______.
3. Emigration - neutrophils push their way ___________.
4. Chemotaxis - movement through CT to ________ and then ________ to _____
5. Opsonization - _________
6. _________ - engulfing of the target
7. Killing - respiratory burst or vacuole degranulation
8. Digestion of dead bacteria/cells
- periphery of blood vessel
- ICAM-1, ELAM-1, GMP-140
- endothelial wall
- out of bloodstream and into CT
- basement membrane
- junctional epithelium
- bacteria
- recognition and attachment to the target
- Phagocytosis
-
Host tissue injury results from _________ and release of _______
- oxygen free radicals
- digestive enzymes
-
Neutrophil Migration - Chemotaxis
- Complement dependent factors
- Complement-independent factors
-
Complement dependent factors
C3a, C5a
-
Complement-independent factors
- Leukotriene
- Products of bacterial metabolism
- Endotoxin -> activated macrophage -> IL-8 (interleukin)
- Tissue injury
-
Neutrophil Granules
- Azurophil (primary): Large, dense; Lysosomal enzymes; Peroxidase (“myeloperoxidase”); Lysozyme (33%); Cationic proteins
- Specific (secondary): Smaller, less dense; Alkaline phosphatase; Lysozyme (67%); Lactoferrin
-
Histopathology of Gingival Disease Described by Page & Schroeder (1977)
- Stage 1 – Initial Lesion
- Stage 2 – Early Lesion
- Stage 3 – Established Lesion
- Stage 4 – Advanced Lesion
-
Initial Lesion (2-4 days)
- Histologic picture of clinically healthy tissue - oral epi
- Microorganisms in the sulcus activate resident leukocytes
- Vascular changes:
- - Dilation of capillaries
- - Increased blood flow
- - Stimulation of endothelial cells
- - Increased vascular permeability allows PMN and monocytes to migrate through CT to bacteria
- Migration of leukocytes into sulcus via chemotaxis
- Increase in flow of gingival fluid into the sulcus
-
Lipopolysaccharide (LPS)
- Outer membrane of G- bacteria, aka endotoxin
- Elicits strong immune response
- Host recognizes LPS via toll-like receptors (TLRs)
- - 1. Increased production of inflammatory mediators (cytokines)
- - 2. Differentiation and recruitment of immune cells
- - 3. Increased vasodilation and vascular permeability
-
Bacterial Waste Products
- NH3
- H2S
- Butyric acid - apoptosis of T-cells, B-cells, Fibroblasts and Epithelial cells
-
Bacterial Enzymes - Proteases
- - Breakdown of CT components, ie. collagen, elastin and fibronectin
- - Gingipains produced by P. gingivalis reduce concentration of cytokines and inactivate TNF-α. Shuts off immune response; causing chronic perioddontitis
-
Microbial Invasion
- invade intercellular spaces of epithelium and connective tissue (Aa, P.g, F. nuc)
- invade epithelial cells and allow other bacteria to enter tissue
- Bacteria in tissues may act as a “reservoir” for reinfection (refractory periodontitis; not responding to treatment; may require chemo)
-
Cytokines - produced by?
Produced by many cells (neutrophils, macrophages, lymphocytes, fibroblasts and epithelial cells)
-
Cytokines - functions
- Key mediators in periodontal disease
- Signaling Proteins
- Bind to receptors on target cells, initiate intracellular signaling resulting in gene expression (alteration of cell’s behavior or secretion of more cytokines) - eg. induces fibroblasts and osteoclasts to produce enzymes to break down CT and bone
- Act in flexible and complex networks, involving pro-inflammatory/anti-inflammatory effects
- Pro-inflammatory cytokines: IL-1β/IL-1α, TNF-α, IL-6
- Important in both innate and adaptive immunity
-
Interleukin-1β
- Produced by monocytes, macrophages, neutrophils, fibroblasts, keratinocytes, epithelial cells, B-cells, and osteocytes
- Stim synthesis of prostaglandin E2 (PGE2) - vasodilation, bone resorption
- Vascular changes, increasing blood flow to site of infection
- Facilitates migration of neutrophils from blood vessel
- Regulates development of antigen-presenting cells, T cells
- Increased GCF concentration in gingivitis/periodontitis
-
Tumor Necrosis Factor (TNF-α)
- Mediates cell and tissue turnover by stimulating MMP release
- Stimulates development of osteoclasts and limits tissue repair by osteoblasts
- Shares many actions of IL-1β
- Increases neutrophil activity - amplification
- Facilitates neutrophil recruitment, IL-1β production, secretion of PGE2
Antagonists of TNF-α, IL-1β -> 80% reduction ininflammation, 60% reduction in bone loss
-
Interleukin-6
- Stimulated by IL-1 β, TNF- α
- Secreted by many immune cells, and osteoblasts to stimulate bone resorption and development of osteoclasts
-
Matrix Metalloproteinases (MMPs)
- Secreted by majority of cell types in the periodontium (fibroblasts, keratinocytes, endothelial cells, osteoclasts, neutrophils, macrophages)
- In health, MMP1 (collagenase) is secreted by fibroblasts to maintain CT hemostasis
- Upregulated by IL-1β, TNF-α
- Also produced by bacteria (Aa, P.g)
- In diseased tissue, MMPs secreted in excessive quantities cause connective tissue breakdown
-
Early Lesion (4-7 days)
- Changes in initial lesion continue to intensify
- Proliferation of capillaries, formation of capillary loops
- Lymphocytes (T-cells) are dominant immune cell present
- Increased migration of PMNs to the epithelium, phagocytosis of bacteria, and release of lysosomes
- Collagen destruction as a by-product apical and lateral to the junctional and sulcular epithelium
- Proliferation of basal cells in order to maintain an intact barrier
- Epithelium proliferates into collagen depleted areas of connective tissue, forming rete pegs
- Less collagen formation near the inflammatory infiltrate
- First clinical signs of erythema, edema, Bleeding upon probing; ulceration of sulcular epithelium, bleeding coming from blood vessels close to the surface
-
Adaptive Immunity
- If innate immunity responses fail to eliminate infection, then the effector cells of adaptive immune response are activated
- Adaptive Immunity involves complex interactions between antigen-presenting cells and T- and B-cells
- Adaptive immune responses initiated in Early lesion and predominate in Established lesions (Plasma cell
- predominate inflammatory cell)
- Non-progressing periodontal lesion are dominated by T
- cells
- Progressing periodontal lesion dominated by Plasma cells
-
___ activate cell-mediated immunity:
- Th1
- Macrophages phagocytose bacteria
- Natural killer cells and CD8 cytotoxic cells kill infected host cells
-
__ regulate humoral (antibody-mediated) immunity:
- Th2
- Antibody production by B-cells
- Release of pro-inflammatory cytokines that further lead to tissue destruction (bone loss in Advanced lesion)
-
Established Lesion (14-21 Days)
- Plasma cell is the predominant immune cell present
- Changes in early lesion worsen
- Continued breakdown of collagen, vascular proliferation, formation of rete pegs
- Moderately to severely inflamed gingiva
- Changes in color, size, texture, consistency, contour of gingiva; no attachment loss
- Gingival lesion is reversible
-
Advanced Lesion
- Extension of the lesion into alveolar bone
- Apical migration of junctional epithelium
- Bone loss
- Loss of attachment
- Clinical signs of acute and/or chronic signs of inflammation may be present
-
Gingivitis precedes Periodontitis. But Not all cases of gingivitis progress to periodontitis despite poor oral hygiene
- Loe, et al 1966
- Sri-Lankan tea laborers who had no access to dental care; Abundant plaque and calculus deposits
- Rapidly progressing group (8%)
- Moderately progressing group (81%)
- Not progressing (11%), only had gingivitis but did not progress to periodontitis
- The major determinant of susceptibility to disease is the nature of the immune-inflammatory response
-
Individuals who are more susceptible to periodontal disease
- an excessive, or dysregulated, immune-inflammatory breakdown
- host and environmental factors that influence and determine progression of disease
- Risk factors such as smoking, systemic diseases (diabetes, nutritional factors), stress
- Genetic polymorphisms may result in hyperinflammatory traits, increasing susceptibility bacterial threshold varies person to person
-
- Microbial challenge at tooth surface, LPS and antigens stimulate host response
- Host response amplified by environmental and risk factors
- Genetic factors play a role as well
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