Pathology Flashcards
Describe the disease process of gingivitis
Bacterial products from plaque stimulate epithelial cells to produce inflammatory mediators.
This causes fluid accumulation in tissues.
This allows neutrophils infiltrate gingival tissues.
Neutrophils release destructive enzymes and other inflammatory mediators.
These mediators cause positive feedback cycles of the disease process
What happens in gingivitis if plaque remains on tooth surface and the host inflammatory response continues?
Inflammation and destruction spreads to all periodontal structures, bone resorption = periodontitis
Why does bone resorption occur in periodontitis?
Create more room for host defence cells
How does the bacterial population shift from health to periodontitis?
From aerobic, gram positive organisms (streptococcal bacteria) to more anaerobic gram negative organisms
How does periodontal disease develop?
Change in environmental conditions causing altered microbial population
Exaggerated inflammatory response
Damage to supporting tissues of teeth
What do environmental changes in periodontal pockets lead to?
Changes in homeostasis of sub gingival microbiota
Altered gene expression
Change in microbial population = dysbiosis
What kind of environmental changes can occur in periodontal pockets?
Sustained plaque = gingival inflammation =
Increased flow of GCF - crevice becomes pockets and environment changes =
Nutrition
Temperature
pH
Oxygen and oxidation-reduction potential
Change from aerobic to anerobic
Why doesn’t everyone get periodontal disease?
Depends on genetics and risk factors e.g. smoking
What 3 factors contribute to periodontal disease?
Microbial dysbiosis, hyper-inflammatory host response and individual patients
How can bacteria directly cause tissue destruction? virulence factors
Leukocyte killing/impairment by leukotoxin (A. actinomycetemcomitans)
Impairment of PMN function
Damage to crevicular epithelium (p. gingivialis, a.a, t. denticola
Breakdown of periodontal tissues by proteolytic enzymes = nutrients for G-ve bacteria
Describe A.A virulence factors
Leukotoxin production = leukocyte killing
Damage to crevicular epithelium
Production of collagenases to breakdown periodontal tissues and providing nutrients for G-ve bacteria
Describe P. gingivialis virulence factors
Damage to crevicular epithelium
Production of collagenases and proteases
Dysregulation of cytokine network
What structure do G-ve bacteria contain that can cause tissue destruction?
LPS = endotoxin - activate complement and bone resorption
Describe the events when plaque accumulates in gingival margin
Infiltration of inflammatory cells which migrate into gingival tissues
Vasodilation and increased capillary permeability to aid this
Increased GCF
Breakdown of collagen in gingival tissue
How soon does an initial periodontal lesion appear after plaque accumulation?
24-48 hours
Describe events involved in an initial periodontal lesion
Patient would appear healthy
Localised to gingival sulcus and adjacent periodontal tissue
Vasodilation and increased vascular permeability
Increased GCF flow
Neutrophils migrate to gingival crevice
Few lymphocytes and macrophages present
How soon does an early lesions appear after plaque accumulation?
4-7 days
Describe events involved in early lesion
Increasing vascularity
Further increased GCF
lymphocytes and neutrophils predominantly infiltrating
Fibroblasts degenerate = more leukocyte infiltration
Collagen destruction = more space
redness of gingival
How soon does an established lesions appear after plaque accumulation?
2-3 weeks
Describe events involved in established lesion
Dense inflammatory cell infiltrate = neutrophils, lymphocytes and plasma cells Further increased GCF More fibroblast damage Loss of gingival collagen NO loss of attachement Formation of pocket
Does an established lesion always change to advanced lesion if plaque is not disrupted?
No - only in susceptible patients
Describe an advanced lesion
Clinical recognised as periodontitis
= pocket, loss of attachments, bone resorption, mobility
Mostly plasma cells in pocket
What mediates the majority fo tissue destruction in periodontitis?
Host immune response
How does the innate immunity contribute to periodontitis?
Saliva
Epithelium
Inflammatory response
How does the innate response present in saliva?
Prevents drying of gignva and teeth
Anti-microbial effects -
- IgA protects mucosal surfaces and prevent adherence
- Swallowing
- Peroxidase = kills bacteria
- lysozyme and lactoferrin weaken cell wall and stop iron binding
How does the innate response present in epithelium?
Physical barrier
Inflammatory response via keratinocytes
Immune response via Langerhans cells (macrophage)
High rate of turnover
junctional epithelium = leaky = release cytokines
How does innate response present in inflammatory response?
Fluid component - GCF
Cellular = neutrophils and macrophages
What does GCF contain?
immune cells Antibodies - IgG, IgA, IgM Complement components Enzymes proteins that activate innate and adaptive immune response at sight of bacterial change
List 4 inflammatory mediators
Cytokines
Prostaglandins
Matrix metalloproteinases
Growth factors
Role of prostaglandins
Bone resorption, neutrophil chemotaxis, vascular permeability and vasodilation
Role of matrix metalloproteinases
Pro-inflammatory, degrade connective tissues
Role of growth factors
Growth factors from osteoblasts which regular osteoclast recruitment
How can adaptive immune response be divided?
Humoral = antibody Cellular = lymphocytes
Role of adaptive immune response
Recognition of specific microbial agents
Release of cytokines
Activation of T and B cells
How can tissue destruction be caused indirectly by host response?
Humeral immunity = activation of complement and increased inflammation, recruitment of inflammatory cells and release of destructive enzymes
T killer cells
Breakdown of bone and collagen = junctional epithelium migrates down
Positive feedback cycle
