Pathogenesis Of Periodontal Disease Revision PDF

Pathogenesis of periodontal disease Chemical mediators = Cytokines, prostaglandins, matric metalloproteinases. Cytokines = Small protein important for controlling immune cell growth and activity. Signal the immune system to aid in inflammatory responses. Acton of cytokines in periodonti...

Pathogenesis of periodontal disease Chemical mediators = Cytokines, prostaglandins, matric metalloproteinases. Cytokines = Small protein important for controlling immune cell growth and activity. Signal the immune system to aid in inflammatory responses. Acton of cytokines in periodontitis = Release pro-inflammatory cytokines in response to pathogens that promotes further periodontal tissue destruction. Prostaglandins = Produced in inflammatory response to periodontitis. Contribute to bone resorption, chemotaxis, vascular permeability and dilation. Matrix metalloproteinases (MMPs) = Family of enzymes, pro-inflammatory response that degrades connective tissue, collagen and other extracellular matrix components. Polymorphonuclear leukocytes (PMNs) = Type of white blood cell, first line of defence in response to protect the body. Include; neutrophils, eosinophils, basophils & mast cells. Bacteria involved in periodontitis & virulence factors P.gingivallis Gingipains - allow use of gingival crevicular fluid for nutrients. Carbohydrate capsule - resist host defences. T.denticola Adherence mechanisms - bind to fibroblasts. Degrades cytokines - disruption of host defences. T.forsythia Proteases and apoptopic factors - causes cell death to immune cells. A.actinomycemcomitans Leukotoxin - destroys white blood cells, inhibits immune response. Proteases and toxins - destroy and invade host epithelial cells. Initial lesion: 2-4 days after plaque biofilm accumulation Bacterial features: Bacteria colonise to tooth surface Cellular features: Junctional epithelial cells release biochemical mediators (Cytokines, matrix metalloproteinases, prostaglandin). Stimulate immune response - Polymorphonuclear leukocytes are recruited - type of white blood cell (Neutrophils, basophils, eosinophils). PMNs pass from blood vessels to gingival connective tissues - PMNs migrate into sulcus to phagocytose bacteria. PMNs release cytokines which can destroy healthy gingival connective tissue which create pathway for PMNs to move quickly to sulcus. Tissue level features: Plaque biofilm location - supragingival. Vascular dilation within dentogingival complex (junctional, sulcular and oral epithelium, connective tissue). Gingival crevicular fluid increases in volume - attracts inflammatory cells to lesion site Clinical features: Gingiva looks healthy clinically Host response: Successful if most bacteria are destroyed - successful host response Body can repair destruction cause by immune system if bacterial infection bought under control (immune system and plaque control). If bacterial pathogens are not controlled, early gingivitis will develop. Early lesion: 4-7 days after plaque biofilm accumulation Bacterial features: Bacteria accumulation continues and biofilm maturation occurs. Production of bacterial toxins and byproducts that penetrate junctional epithelium. Cellular features: Migration and chemotaxis of PMNs (PMNs leave blood vessels and move towards site of inflammation). Cytokines released by junctional epithelium in response to increased bacteria - attract more cellular defenders. Cytokines released by PMNs - cause local destruction of connective tissue - allows for more PMNs to migrate through tissue towards sulcus. Increased permeability of blood vessels - allows large numbers of PMNs to move to gingival connective tissue near infection site. PMNs phagocytose bacteria in sulcus to protect host tissues from bacteria - destroy healthy gingival connective tissue as they rush to sulcus. Wall of cells between biofilm and sulcus are formed by PMNs at junctional epithelium Macrophages are recruited to connective tissues - release biochemical mediators (cytokines, matrix metalloproteinases, prostaglandins) Biochemical mediators - recruit more immune cells. MMP degrades collagen in afffected connective tissue. T lymphocytes migrate to connective tissue - produce cytokines and antibodies. Tissue level: Sulcular epithelium and adjacent connective tissues are most affected - collagen loss of 60-70%. Sulcular epithelium starts forming epithelial ridges due to inflammatory changes. Junctional epithelium cells start to proliferate (increase in number). Clinical features: Edema (fluid build up, inflammation) and redness of gingival marginal tissue is observed clinically. Reversible. Host response: PMNs, macrophages, T-lymphocytes in large numbers - may control bacterial pathogens. Good patient oral hygiene can disrupt plaque biofilm and result in return to health if bacterial infection bought under control - body can repair destruction caused by immune response. If host response fails, early lesion will progress to established gingivitis. Established lesion: 21 days after plaque biofilm accumulation Bacterial features: Plaque biofilm extends subgingivallly into gingival sulcus. Disrupts attachment of coronal portion of junctional epithelium from tooth surface. Cellular features: Migration to additional cellular defenders to site. Sub gingival bacteria stimulate epithelial cells to secrete more cytokines — more recruitment of PMNs, macrophages, lymphocytes. Plasma cells - main element in affected connective tissue (leukocytes that produce antibodies). Larger quantities of antibodies produced by plasma cells - assist in controlling bacteria. Immune cells send more immune cells to fight bacteria. More toxic chemical released - more healthy connective tissue destroyed. Cytokines are produced by macrophages and recruit additional macrophages and lymphocytes. Prostaglandin and matrix metalloproteinases - start collagen destruction. Gingival fibroblasts - stimulated to produce more prostaglandin and matrix metalloproteinases - more collagen destruction. Tissue level: Epithelial ridges extend deeper into gingival connective tissue - maintain epithelial integrity. Junctional epithelium attachment loosens - starts to transform into pocket epithelium - thinner and more permeable. More collagen loss - within connective tissue occupied by inflammatory cells. Clinical features: All usual features of gingivitis evident - more noticeable compared to initial stage. Reversibe. Host response: Host response can be adequate to contain bacterial challenge in this phase. PMPR and oral hygiene education can be helpful - stop bacterial challenge and return periodontium to health. If bacterial infection not controlled, will progress to periodontitis. Advanced lesion: Periodontitis Bacterial features: Plaque biofilm grows laterally and apically along root surface. Periodontal pocket provides ideal environment for continued growth of subgingival bacterial - chronic and repeated challenge for host. Cellular features: Host response intensifies. Bacterial infection becomes chronic - causing chronic inflammation. Immune response so intense that it starts to harms the periodontium (cementum, PDL, alveolar bone and gingivae). Cellular defenders intensify defence against bacteria pathogens. PMNs, macrophages and epithelial cells - produce cytokines - cause destruction of gingival connective tissue and PDL fibres. Macrophages - produce large amounts of cytokines, postaglandin and matrix metalloproteinases - destruction of connective tissue and alveolar bone. MMPs control the destruction of extracellular matrix, collagen and periodontal ligament. Prostaglandin mediates destruction of alveolar bone - stimulates large number of osteoclasts to resort the crest of alveolar bone. Gingival pocket progresses to periodontal pocket. Tissue destruction becomes main outcome of immune system response - overwhelms any tissue repair. Tissue level: Destruction of periodontal tissues occurs. Junctional epithelium cells migrate apically - development of periodontal pocket. Gingival fibroblasts shift to state that favours gingival connective tissue and PDL fibre destruction. Osteoclasts destroy alveolar bone crest. Clinical features: Periodontal pocket formation, bleeding on probing, PDLL destruction, alveolar bone loss, furcation involvement, tooth mobility. Irreversible changes. Host response: Chronic inflammation due to chronic infection - destroys periodontal tissues and more causes more damage to periodontium than bacterial infection. Irreversible tissue damage marks periodontitis. Factors that may influence host response: Abnormal PMN function - increases risk of infection. Persistence in virulence factors of bacteria within plaque biofilm. Acquired and environmental factors - smoking, stress. Systemic factors - uncontrolled diabetes and genetic factors.