Perio

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bbberg
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Perio
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2012-05-25 03:49:59
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Exam 1
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  1. Etiological agents for progressive periodontitis
    • Porphyromonas gingivalis
    • Tanerella forsythia
    • Aggregatibacter actinomyetemcomitans
  2. Periodontitis as a manifestation of a systemic disease
    • Onset is eruption of 1st teeth
    • Occurence is rare
    • Acute inflammation
    • Defects in PMNs/monocytes
    • Frequent infections
    • 1st and permanent teeth affected
    • Systemic problems
    • Papillon-LeFevre is example
    • Patients with generalized PMN defects are at clear risk for periodontitis and are more susceptible to bacterial infections
  3. Myeloid lineage gives:
    Neutrophils from myeloid stem cells
  4. Initial lesion
    • Slightly elevated vascular permeability and vasodilation
    • GCF flows out of sulcus
    • Migration of leukocytes (mainly PMNs) in relatively small #s through gingival CT across JE and into sulcus
    • Epithelial cells are 1st to sense microorganisms on surface
  5. Early lesion
    • Corresponds to early gingivitis that is evident clinically
    • Increased vascular permeability, vasodilation, and GCF flow
    • Large #s of infiltrating leukocytes (mainly PMNs and lymphocytes)
    • Degeneration of fibroblasts (creates room for leukocytes to get to bacteria quickly)
    • Collagen destruction
    • Proliferation of junctional and sulcular epithelium into collagen depleted areas
  6. Established lesion
    • Corresponds to established, chronic gingivitis
    • Dense inflammatory cell infiltrate (plasma cells, lymphocytes, PMNs)
    • Accumulation of inflammatory cells in CT
    • Elevated release of Matrix Metallo-Proteinases and lysosomal contents from neutrophils
    • Significant collagen depletion and proliferation of epithelium
    • Formation of pocket epithelium containing large numbers of neutrophils
  7. Advanced lesion
    • Marks transition from gingivitis to periodontitis
    • Predominance of PMNs in pocket epithelium and pocket
    • Dense inflammatory cell infiltrate in CT (mainly plasma cells)
    • Apical migration of JE to preserve intact epithelial barrier
    • Continued collagen breakdown resulting in large areas of collagen depleted CT
    • Osteoclastic resorption of alveolar bone (to create more vessels, to bring in more cells to deal with bacteria)
  8. Microbial virulence factors are essential for
    survival of microorganisms
  9. What destroys bone?
    Body NOT bacteria
  10. Bacterial infection depends on
    • Attachment to host cell
    • Proliferation of organisms
    • Avoidance of phagocytosis
    • Damage to host cell
  11. Porphyromonas gingivalis (Pg) is recognized by:
    • Associated with periodontal disease - when disease goes away so does microorganism
    • Fimbriae (molecules on surface of microorganism that give it the ability to adhere)
    • Capsular polysaccharides (different from ones we make so body knows they are foreign)
    • Hemagglutinin
    • Lipopolysaccharides (LPS)
    • Enzymes
    • Protein antigens
  12. Pg LPS
    • atypical LPS lacks of 2keto3deoxyoctonate
    • Little endotoxic but high mitogenic activity for B cells
    • In AP and LJP mostly IgG2 then IgG1>IgG3>IgG4
  13. Pg Enzymes
    • Major virulence factors
    • Degrade serum proteins, Ig and complement C3 (prtH gene)
    • Prevent phagocytosis
    • Thiol-dependent collagenase 35kDa (prtC gene) - have collagenases but not responsible for tissue destruction
    • Lives on proteins, not sugar
  14. Pg Gingipains
    • Trypsin like proteases (thiol dependent and non-thiol dependent) with very narrow specificity
    • Cysteine gingipain (prtT gene)
    • Arginine-gingipain (RgpA and RgpB)
    • Lysine-gingipain (Kgp)
  15. Aggregatibacter actinomycetemcomitans (Aa)
    • Serotype specific carbohydrate
    • LPS
    • Leukotoxin (most dangerous toxin produced by Aa)
    • Fimbriae
    • Protein antigens
    • Pts with this bacteria have a lot of bleeding and bone loss
  16. Aa Leukotoxin (LT)
    • Aa stain JP2
    • Cytotoxic for human PMNs
    • Localized early onset periodontitis pt have neutralizing antibodies to LT but don't help the killing of Aa
  17. Inflammatory mediators
    • Transendothelial migration
    • Chemotaxis
    • Phagocytosis
    • Antigen processing and presentation
    • T and B cell responses
  18. Microbial interactions with the host in periodontal diseases
    • Adherence, evasion to host response, tissue invasion
    • Innate immunity: complement activity and phagocytes
    • Acute inflammation: neutrophils (aggressive periodontitis)
    • Chronic inflammation: T cell lesion vs B cell lesion (gingivitis and chronic periodontitis)
    • Tissue destruction: proteinases
  19. Innate Immunity
    • Barriers
    • Cellular: phagocytes and PMNs
    • Humoral: complement
  20. Adaptive Immunity
    • Cellular: T and B cells
    • Humoral: Antibodies
  21. Complement
    • Central component is C3
    • Goal of complement system is formation of C3b
    • Both alternative and classic pathways lead to formation of C3 convertase enzymes and generation of C3b
    • Biologic consequences of C3b formation depend on presence/absence of regulators
    • Produced in liver, circulate in blood
  22. Transentothelial migration and chemotaxis
    • Rolling: L-selectin constitutively expressed
    • Increased rolling: P-selectin expressed with E-selectin introduced
    • Chemokine signal: IL-6 expressed by stimulated endothelium
    • Rolling arrest: L-selectin shed, LFA-1 expressed, interacts with ICAM2 on endothelium
    • CD31 zipper
  23. PMNs and other leukocytes can hone in on irritants
    • By chemotaxis
    • Requires chemotaxin receptor
    • 7 transmembrane domains, 3 extracellular loops, 3 cytosolic loops
    • G protein coupled
    • Neutrophils polarize (anterior lamellipod, posterior uropod)
    • Cytoplasm appears to squirt through contractile ring
    • Can detect 1% gradient over length of its cell body at nanomolar concentrations
  24. Acute Inflammation
    • Innate immunity
    • Cellular is PMNs and phagocytes: proteinases, cytokines/chemokines, prostaglandins
    • Humoral: complement (chemotaxins C5a, C3a, C4a) are small fragments that become soluble upon activation
  25. Why are neutrophils so important against periodontal pathogens?
    We don't know
  26. Neutropenia
    • Low PMN counts
    • Agressive and extensive inflammation in gingival tisues
    • Leads to inflammation and advanced attachment loss
    • LAD1 involvs defects in neutrophil transendothelial migration resulting in a lack of extravascular neutrophils in periodontal lesions
    • With LAD dense infiltrates of mononuclear leukocytes are found in periodontal lesions and extensive bone loss is seen
  27. Neutrophil abnormalities leading to aggressive periodontitis
    • Neutropenia, agramulocytosis, Chediak Higashi Syndrome
    • Papillon-LeFevre Syndrome (thick keratin on hands and feet)
    • Leukocyte Adhesion Deficiency Type 1 (LAD 1)
    • Leukocyte Adhesion Deficiency Type II (LAD II)
  28. Dendritic cells (DC) are link between innate and adaptive immunity
    • Pathogen associated molecular patterns (PAMP)
    • Chemotaxis--> Initiate phagocytosis (pattern recognition receptors) --> Oxygen reduction (NADPH oxidase) --> Killing (H2O2 + Cl --> HOCl)
    • Process of neutrophils
    • Chemotaxis: mobility that enables leukocyte to locate targe
    • Phagocytosis: involves receptors with ligands which coat offending particle or cell
    • Oxygen reduction: formation of some oxygen metabolites can kill some bacteria
    • Killing: traps in phagosome, fuse with lysosome, forms hypochlorous acid (HOCl)
  29. Phagocytic cells, dendritic cells, and macrophages (BUT NOT PMNs) are the link between innate and adaptive immunity
  30. Mononuclear Phagocytes - Antigen processing, presentation and co-stimulation
    • Phagocytes closely related to neutrophils
    • Exhibit chemotaxis, phagocytosis, and killing
    • Particularly adept at processing and presenting antigen to T cells
    • Requires more than 20 hours
    • Release cytokines
    • Direct lymphocyte differentiation
  31. Exogenous pathway
    • Extracellular microorganisms are phagocytosed
    • Destroyed and reduced in peptides
    • Presented to T cells via MHC Class II molecules
  32. Co receptor CD4
    Works with antigen presenting cell (Is CD4 T helper cell)
  33. Costimulation
    • Very important
    • TCR-MHC peptide interaction is necessary butnot sufficient to activate T cells
    • B7/CD28 interaction is also needed for the activation of T cells
    • Phagocytosis and breakdown of bacteria by macrophage induces expression of MHC Class II and B7
    • Macrophage delivers a co-stimulatory signal to T cells recognizing bacterial peptide antigen
    • Proliferation and differentiation of T cells specific for bacterial protein
  34. T cell proliferation
    • Clonal selection --> Clonal Expansion --> Clonal contraction --> Memory
    • Protective immunity is acheived if an adequate number of the lymphocytes are maintained in the memory phase
  35. T cell differentiation
    Dendritic cells and macrophages --> Antigen presenting cell--> Ag-MHC Class II --> Th0 --> either Th1 (Responses against intracellular changes) or Th2 (responses against extracellular changes)
  36. T cell subsets
    • Effector T cells (Th 1, 2, Th17)
    • Regulatory T cells (Foxp3+, Foxp3-) - adaptive and natural
  37. Th17 cells appear to
    • ILs--> Fibroblasts, macrophages, endothelial cells, epithelial cells --> anti-microbial peptides--> Pathogen killing
    • Also neutrophil induction--> pathogen killing
  38. Susceptibility for periodontal disease
    • 50% genetic
    • 50% environmental
  39. Prostanoids are lipid mediators of
    • Inflammation: Prostaglandins, Thromboxans, Leukotrienes
    • Resolution: Lipxins, Resolvins, Protectins (helps reduce inflamamtion, being marketed in toothpastes to help dampen inflammation and therefore mediate periodontal disease)
  40. Linoleic acid in plasma membrane
    • Delayed mediators of inflammation
    • Block phospholipase C (with steroids) or cycloxygenase pathway (with NSAID like asprin/ibuprofen) to block inflammation
  41. Th1, Th2, and Th17 in periodontal disease
    • Th1: cytokine IFNgamma protects from bone loss
    • Th2 cytokines IL10, IL6, and IL4 don't protect from disease
    • Th17 activate neutrophil mediated defenses - protective or detrimental?
  42. Bacterial challenge in periodontitis
    • Acute inflammation (PMNs)
    • Immune response phase (Th1, Th2, Th17)
    • Resolution phase or
    • Bone destruction phase
  43. Cells in periodontal tissues
    • Gingivitis lesion: maintly Th1 lymphocytes and constant flow of PMNs
    • Periodontitis lesion: mainly activated B cells and plasma cells
    • Activation of B cells is dependent on Th2 lymphocytes
  44. Destruction Phase
    • Cytokine production most important IL-1B but also TNFalpha, IL6, IL8, IL12, IL15, and chemokines MCP1 and RANTES
    • Cytokine induced alteration of the CT metabolism
    • Inbalance between collagenases and matrix metalloproteinases (MMPs) activity and collagen synthesis
    • IL1 and IL6 induce fibroblast and osteoclast activation
  45. Induction of bone loss
    • Osteoclast progenitors express the receptor activator NFkB (RANK)
    • Activated T cells express the receptor activator of NFkB Ligand (RANKL)
    • RANK/RANKL interaction + MCSF generates Tartarate-Resistant Acid Phosphatase positive (TRAP+) osteoclasts --> Bone resorption
  46. Osteoprotegrin
    • Acts as a decoy receptor that prevents RANKL from binding to its receptor RANK on precursor cells
    • Blocks: Monocyte--> Precursor cell (RANK, waiting for RANKL to activate) --> bone resorption
  47. RANKL
    • Is present within gingival tissues in periodontitis
    • Activated T and B cells express the receptor activator of RANKL
    • Expression higher in disease
  48. Chronic gingivitis
    • Inflammation of gingiva
    • Comes on slowly, is of long duration, and is usually painless
    • Most common type
  49. Acute Gingivitis
    • Inflammation of gingiva
    • Comes on rapidly and is of short duration
  50. Color of gingiva
    • Normal = pink
    • Diseased = red (erythmatous) or bluish red
  51. Size and shape of gingiva
    • Normal = knife edge margins
    • Diseased = swollen (edematous)
  52. Consistency of gingiva
    • Normal = firm, resilient
    • Diseased= soft, friable
  53. Texture of gingiva
    • Normal= stippled
    • Diseased= loss of stippling, smooth, shiny
  54. Distribution of gingivitis
    • Localized
    • Generalized
    • Marginal
    • Papillary
    • Diffuse
  55. Types of Gingivitis
    • Necrotizing ulcerative gingivitis
    • Acute herpetic gingivostomatitis
    • Pericoronitis
    • Acute periodontal abscess
    • Desquamative gingivitis (not bacterial)
  56. Pericoronitis
    Incompletely erupted tooth surrounded by inflammation
  57. Desquamative gingivitis
    • Desquamation of epithelium
    • Intense redness
    • Gingiva and mucosa involved
    • Autoimmune disease
  58. Herpetic Gingivostomatitis
    • Etiology= viral (herpes simplex)
    • Erythema
    • Vesicular eruption (almost always on attached gingiva)
    • Painful
    • Children
    • Duration 7-10 days
  59. Gingival Hyperplasia
    • Phenytoin (20-50%)
    • Cyclosporine (10-20%)
    • Ca-channel blockers (10-25%)
  60. Drug induced gingival enlargement
    • Anticonvulsants
    • Immunosuppresive agents
    • Calcium channel blockers
    • Sex hormones
    • Discontinue drug (if possible)
    • Surgical reduction of tissue
    • Frequent prophylaxis
    • Strict oral hygiene
  61. Periodontitis
    • Inflammation of the supporting tissues of the teeth
    • Destructive change leading to loss of bone and periodontal attachment
  62. Clinical features of periodontitis
    • Fetid odor
    • Itching gums
    • Usually painless
    • Loose teeth
    • Migration of teeth
    • Gingival bleeding
    • Bluish or red gingiva
    • Pocket
    • Bone loss
    • Attachment loss
  63. Modes of progression of periodontitis
    • Progressive loss (long period)
    • Random burst (long period)
    • Multiple burst (short period)
  64. Classification of pockets
    • Gingival pocket (pseudo or relative)
    • Periodontal pocket (subrabony/supracrestal or infrabony/subcrestal) - true or absolute pocket
  65. Types of infrabony pockets
    • 3 osseous walls
    • 2 osseous walls
    • 1 osseous wall
    • 4 osseous walls
  66. Periodontal pockets
    • Suprabony: base of pocket coronal to crestal bone - pattern of destruction is horizontal, transseptal fibers are horizontal, supracrestal fibers follow normal bone contour
    • Infrabony: base of pocket apical to crestal bone - pattern of destruction is vertical or angular, transseptal fibers are oblique, supracrestal fibers follow angular pattern of osseous defect
  67. Periodontal Pocket
    • Simple
    • Compound
    • Complex
  68. 2 most significant risk factors in determining how at risk a person is for oral cancer and periodontal disease are:
    • Tobacco use
    • Genetics
    • IL1 genotype positive 3x more likely to lose teeth
    • Smoker is 3-5x more likely to lose teeth
    • Both is 8x more likely to lose teeth
  69. Oral cavity related risks of smoking
    • Pregnant women who smoke have increased risk of triggering development of cleft lip/palate in their child
    • Children exposed to secondhand smoke (ETS) have more caries in their deciduous teeth
    • ETS can delay development of permanent teeth by as much as 4 months
  70. Cleft lip/palate
    • Develops within 5-8 weeks of conception (often before mother is aware of pregnancy)
    • An infant with a specific gene whose mother smokes during pregnancy is 6x more likely to get cleft lip/palate
  71. Secondhand smoke and caries
    • 53% had serum continine levels were consistent with secondhand smoke exposure
    • Elevated serum continine levels are significantly associated with an increase in both decayed and filled deciduous (but not permanent) teeth
    • 27% of the children who have caries in deciduous teeth could be caries free if ETS were eliminated
  72. Incidence of leukoplakia and recession
    • Leukoplakia in spit tobacco users (ST)= 50-60%
    • Gingival recession: 25-30%
  73. Incidence of dysplasia or carcinoma
    • Leukoplakia: 5%
    • Erythroplakia: 90%
    • >90% of the lesions occur at the site where the quid is held
  74. Other health implications of tobacco
    • ST may be a risk factor for severe active periodontal disease
    • ST use is associated with risk factors for cardiovascular disease (elevated blood pressure and cholesterol levels)
  75. Smoking is a major risk factor for periodontal diseases
    • both current and former smokers have an increased prevalence and severity of periodontal diseases
    • Gingiva tend to be fibrotic with thickened rolled margins
    • Minimal gingival redness or edema relative to disease severity
    • Proportionately greater pocketing in anterior and maxillary anterior segments
    • Gingival recession in anterior segments
    • Relatively severe and widespread disease compared to a person of the same age who never smoked
    • No association between periodontal status and plaque or calculus scores
  76. Local effects of tobacco use
    • Gingival vasoconstriction
    • Cytotoxic effects on cell proliferation and metabolism
  77. Systemic effects of smoking
    • Immunosuppresion: alters PMN chemotaxis and phagocytosis, impaired serum antibody response
    • Impairment of soft tissue and bone cell function: may interfere with fibroblast attachment, may be associate with reduction of skeletal mineral content
    • Immunology: altered PMN chemotaxis/phagocytosis, increased TNFa and PGE in GCF, increased neutrophil collagenase and elastase in GCF, increased production of PGE by monocytes in response to bacterial LPS
  78. Wound healing due to tobacco
    Impaired wound healing and less-favorable clinical outcomes to both non-surgical and surgical periodontal therapy of smokers vs. non-smokers
  79. Periodontal Tx Results
    • Nonsurgical - reduced response to S/RP and locally delivered antibiotics, less reduction in pocket depths, less gain of clinical attachment levels
    • Surgical - Less pocket reduction and less gain of clinical attachment levels, open flap debridement, osseous resection, bone grafting, less success with gingival grafts
    • Guided tissue regeneration (GTR)- less gain of clinical attachment level, less bone fill, increased recession, increased membrane exposure
  80. Implant failure rates in smokers are 2x non-smokers
    A higher failure rate of the maxillary arch accounts for majority of difference
  81. Odds of periodontal disease due to ETS
    Adjusted odds of having periodontal disease is 1.6x greater for non-smokers exposed to ETS than for those not exposed
  82. Impact of smoking on wound healing
    • Smoking impairs revascularization of bone and soft tissue
    • PMN altered chemotaxis, phagocytosis, adherence
    • Altered antibody production (less serum IgG concentration)
    • Many tobacco components may be toxic to cells (impaired fibroblast attachment)
    • Negative effect on bone metabolism (may influence osteoporosis and periodontosis by similar mechanisms)
  83. Treatment results of smokers
    • Former smokers and those who have never smoked appear to respond equally well to tx
    • Tx results are not as effective in smokers compared to non-smokers
    • BUT periodontal therapy improves periodontal parameters in both smokers and non-smokers
  84. Benefits of smoking cessation
    • Periodontal status stabilizes for a majority of patients and attachment loss ceases or slows
    • Risk of periodontitis decreases with the incresase in the number of years since quitting
  85. Tobacco industry
    Tobacco is least regulated consumer product in US
  86. Nicotine is
    • 1000x more potent than alcohol
    • 10-100x more potent than barbituates
    • 5-10x more potent than cocaine or morphine
  87. Nicotine combines with neurotrainsmitters in brain
    • Dopamine: pleasure, suppress appetite
    • ACh: Arousal, cognitive enhancement
    • Serotonin: Mood modulation, suppress appetite
    • NE: arousal, suppress appetite
    • Vasopressin: memory improvement
    • Beta endorphin: reduce anxiety/tension
  88. Criteria for nicotine withdrawl
    • Depressed mood
    • Insomnia
    • Irritability, frustration, or anger
    • Anxiety
    • Difficulty concentrating
    • Restlessness
    • Increased appetite or weight gain
  89. Addiction and alcoholism
    • 80-90% of alcoholics are heavy smokers
    • Active alcoholics are less likely to succeed in quitting than smokers with no hx of alcoholism
  90. Nicotine addiction
    • 30-50% of smokers have a hx of depression
    • NIcotine may act as an antidepressant in some smokers
    • 30-50% of MI patients continue to smoke
    • 63% of smokers who undergo surgery to clear blocked vessels continue to smoke even though smoking after surgery "substantially reverses and benefit gained from the procedure"
  91. Stages of change
    • Precontemplation
    • Contemplation
    • Preparation for Action
    • Action
    • Maintenance
    • Relapse
  92. Relapse
    • Intensity of tobacco withdrawl symptoms often peaks during the first week post quit
    • About 65% of self quitters relapse during the 1st week
  93. 5 As of Quitting
    • Ask
    • Advise
    • Assess
    • Assist
    • Arrange
  94. Chronic gingivitis
    • Gram + actinomyces increase
    • Gram - 25-45% fusobacterium species, prevotella intermedia
  95. NUG/NUP
    • Sudden onset
    • Punched out papilla
    • Pseudomembranous slough
    • Fetid odor
    • Painful
    • Elevation in temp
    • Lymphadenopathy
    • Etiology- bacteria
    • Spirochetes, fusobacteria
    • Prevotella intermedia, fusobacterium species
  96. Gingivitis associated with pregnancy
    • Anaerobic bacteria
    • Prevotella intermedia
  97. Chronic periodontitis
    • Onset 30
    • No PMN or monocyte abnormality
    • Disease generalized
    • May convert to rapid progressive
    • Bone loss variable
  98. Periodontitis
    • Gram - 75%
    • Anaerobic
  99. Refractory Periodontitis bacteria
    • Porphyromonas gingivalis
    • Tannerella forsytha
    • Prevotella intermedia
    • Campylobacter rectus
    • Enterics
    • Actinomyces and streptococcus
  100. Localized Aggressive Periodontitis
    • Defect in PMN chemotaxis
    • Females 3-4x more likely
    • Lesions are 1st molars/incisors
    • Pubery - 25 years
    • Familial
    • Gram- 65% - Aa

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