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95 Cards in this Set
- Front
- Back
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Epidemiology
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The study of distribution and dynamics of diseases in a human population.
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Objectives of Epidemiology
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Identify:
- Risk factors or indicators - Which populations are at high or low risk - Trends of Disease patterns |
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Epidemiologic Indices Characteristics
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-Simple to use
-Reproducible -Amenable to statistical analysis -Defined clinical conditions objectively |
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Indices used in study of periodontal diseases
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Plaque accumulation
Calculus accumulation Gingival inflammation Periodontal destruction |
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Prevalence vs Incidence
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- The portion of individuals affected by a disease at a specific point in time
- The rate of occurance of new disease in a population in a given time period |
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Gingival Index
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-Gingival Units include facial margin, distofacial papilla, mesiofacial papilla, entire lingual surface
-Assess the severity and location of gingivitis -Use a probe to see bleeding potential. 2 = bleeding |
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Gingival Index Score & Plaque index score
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Mean Gingival index score per tooth = total gingival index scores /4
Gingival index score per person = total mean gingival index scores/number of teeth |
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Plaque Index
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- Gingival margins
- Determine location and severity of plaque accumulation - Use mouth mirror & explorer |
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Volpe-Manhold Calculus Index
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-Assess quantity of supra gingival calculus
-Use probe to measure lingual of six mandibular incisors -Often used in longitudinal studies to assess treatment efficacy |
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Periodontal disease index
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-Assess quantity of periodontal destruction present
-Involves both gingival inflammation and attachment loss -Teeth measured include 3,9,12,19,25,28 |
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Procedure for measuring periodontal disease index
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Examine all four gingival surfaces to determine gingivitis score
Highest is recorded for gingivitis Clinical attachment is measured at mid facial to mesial surfaces Highest score is recorded and gingivitis score is tossed |
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Periodontal disease index score per person
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Total of scores/# of teeth
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Risk assessment
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Risk factor - Environmental, behavioral or biologic factor which if present, directly increases probability of disease occuring, and if removed reduces the probability
Risk indicator - Probable or putative risk factor that has not yet been confirmed by longitudinal studies |
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Epidemiology of PD
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-Early onset periodontitis is 1% in industrialized contries
- Prevalence of moderate adult periodontitis is 44% ranging from 16-80% for ages 18-64 -Advanced adult PD is 10-15% -In the US, 20 million have advanced PD |
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Risk factors associated with PD
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Smoking
Diabetes Actinobacillus actinomycetemcomitans, porphyromonas gingivalis, bacteroides forsythus -aging, gender, genetics, stress, systemic diseases, nutrition |
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Papillon Lefevre Syndrom
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Autosomal recessive disorder
Deficiency of Cathepsin G Palmoplantar hyperkeratosis Severe early onset periodontitis |
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Factors in PD
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IL1-B activates osteoclasts
Inc MMP Dec Collagen II, IL-10 antagonizes IL1b and TNFa |
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Periostat
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Low levels of doxycyclin can inhibit MMPs to treat periodontal disease
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Interaction between DC & T cells
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Three signals
MHC antigen with TCR CD28 with CD80/86 IL-12 |
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TH1/2
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1- Destroys tumors & virally infected cells
2- Humoral responses |
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Tregs & Th17 responses
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Tregs prevents autoimmune diseases caused by TH17 releasing IL17 that induces PMNs, osteoclasts, defensins.
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CD1a
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Cell markers for Immature DCs, Langerhans cells
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CD83
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Cell markers for Mature DCs, germinal center DCs
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How does Porphyromonas Gingivalis invade CD1a & DCs, what is consequence?
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Invades epithelium via fimbriae which are readily taken up by DCs. Induces DC maturation & Costimulatory molecule expression for T cell priming.
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Characteristics of Biofilms (6)
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-Communities of bacteria evolved to allow survival of community
-Metabolic cooperativity -Primitive circulatory systems -Numerous microenvironments with diff pH, O2 conc, and electric potential -Resistant to host defenses -Resistant to locally delivered antibiotics & antimicrobials |
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Classification of Plaques
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Supragingival - Dental, Marginal
Subgingival - Dental, unattached, sulcular/junctional epithelial associated plaque |
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Formation of dental plaque (3)
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-Adsorption of salivary pellicle coating on tooth surface
-Initial adherence & colonization - Secondary colonization, bacterial growth & Plaque maturation |
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Biological importance of plaque
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- Used for epidemiological studies to monitor oral hygiene and PD
- Experimental studies in germ-free animals for suspected pathogens of PD -Longitudinal case studies |
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Clinical manifestations of gingival index
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1=inflammed 2=bleeding upon touching
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Soft accumulations of bacteria & tissue cells that lack organization and is easily displaced by water
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Materia alba
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Calculus
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Hard deposit formed by mineralization & covered by a layer of unmineralized plaque
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Does calculus cause PD?
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No biofilm does
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Components of calculus
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Hydroxyapetite
Brushite Whitlockite Octacalcium phosphate |
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Supragingival Calculus
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-Located coronal to gingival margin
-White or whiteish yellow from food or tobacco stains -Facial of M1 and lingual of mand incisors |
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Subgingival calculus (4)
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-Below crest of marginal gingiva
-Hard & dense -Appears brown -Stained by gingival fluid |
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Etiological significance of Calculus (4)
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-It is not the main etiological factor in development of PD
-Contributing factor to disease progression -Keeps plaque in close contact to gingiva -harbors plaque & creates places where plaque removal is impossible |
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Opportunistic vs Specific Infection
PD? |
Opportunistic is overgrowth of part of biofilm
PD is opportunistic & Association |
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3 Characteristics of people with periodontitis
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-Succeptible host
-Increase in periodontal pathogen (In # & Proportion) -Decrease in beneficial species |
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Criteria for determination of Microbial Etiology (5)
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1. Association
2. Elimination 3. Host response 4. Animal Pathogenicity 5. Biochemical Determinants |
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2 Characteristics of Healthy Periodontium
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1. Little Plaque
2. Mostly Gram Positive bacteria Streptococcus & Actinomyces |
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Flora in Gingivitis
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-Increase in plaque & subgingival microflora
-Gram Positives still predominate -Gram negatives increase Fusobacterium Nucleatum Bacteriosides Intermedius Capnocytophaga Sp |
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Steroid Hormone Induced gingivitis
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-Associated with Puberty, Pregnancy, Steroid drug therapy, Birth control
-Prevotella Intermedia is elevated in this type of gingivitis (Thrives on Steroid hormones) -Can progress to pyogenic granuloma |
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Gingivitis during Pregnancy
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- Highest during second trimester.
- Five fold increase in Prevotella Intermedia |
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Systemic factors leading to Chronic Periodontitis
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Diabetes Mellitus
HIV |
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Microorganisms associated with PD
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Red Complex
-Porphyromonas Gingivalis -Bacteriosides Forsythus *Gram Neg Anarobes -Troponema Denticola (Spirochete) |
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Advanced disease with minimal clinical inflammation
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Can be caused by gram-negative rods
Bacteroides Intermedius Eikenella corrodens |
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NUG
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Necrotizing Ulcerative Gingivitis
-Invasion of connective tissue by spirochetes -Prevotella Intermedia & Fusobacterium Nucleatum are present |
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Aggresive Periodontitis common characteristics
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- Diseased sites infected with actinobacillus actinomycetemcomitans
-Abnormal phagocytic function -Hyperresponsive macrophages producing excessive IL1B & PGE |
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Aggresive PD types & characteristics
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Localized Form:
- Circumpubertal onset - Localized attachment loss on atleast 2 permanent teeth, one of which is a first molar. Affecting molars & Incisors -Robust serum antibody response Generalized Form: - Usually affecting ppl under 30 - Affecting atleast 3 teeth other than first molars & incisors - Episodic nature of destruction - Poor serum antibody response |
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NUP
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-Characterized by necrosis of gingival tissues, PDL, and bone
-Associated with HIV, Immunosupression, malnutrition |
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Inflammatory cell infiltrate in PD
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First line: PMNs
Second: Macrophages & weak APCs -Dendritic cells bridge innate-adaptive |
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Eicosanoids
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-Includes Prostaglandins, Prostacyclins, Thromboxanes & Leukotrienes
-Platelet aggregation -Vasoconstriction & Dilation -Neutrophil chemotaxis -Inc vascular permeability |
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PGE2 & PD
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-Increases MMP secretion
-Inc osteocalcic bone resorption -Acts alongside TNFa and IL-1 synergistically |
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Advantage of separating Chiral NSAIDS
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-May provide greater efficacy
-Lower dose needed -Less side effects -Patents = money |
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Adverse affects of NSAIDS
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-GI upset & Hemmorhage
-Renal & Hepatic impairment -Allergic reactions -Blood & Bone Marrow damage -CNS disturbances |
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Future considerations in utilizing NSAIDS in PD
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-ID major pathway of disease progression
-ID the most effective combo of NSAIDS -Most effective dose -Idea delivery system -Primary treatment vs adjunctive treatment |
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Challenges of Host Modulation
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-Results of acute animal models are not predictive for chronic human disease
- Acute vs chronic responses not clearly understood - Target for chronic phase may be diff - Toxicity could be issue - Different expectations |
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Reasonable expectation of success for PD therapy
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-Reduced local & systemic inflammation
-reduced probing depths and Reattachment -Longitudinal effects - New bone & dentition saved |
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Hallmark of PD
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CD83+ mature dendritic cells in lamina propria
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GCF
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Fluid obtained from the gingival sulcus that is independent of the major salivary glands and whose volume, composition and flow rate are directly proportional to degree of inflammation
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GCF origin
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Modified inflammatory exudate secreted from the crevicular plexus in the post capillary venules sub-adjacent to JE.
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GCF collection
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Micropipets - 5 min
Filter strips - 5 seconds |
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Measurement of GCF
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Weight - 0.1mg/3min
Stain - Ninhydrin area Microscopy - grid/calibrated squares Electronic meter - Periotron, capacitance to fluid volume |
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GCF composition
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-Cells
-Electrolytes -Organic compounds -Metabolic compounds -Enzymes |
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GCF Cell composition
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-Desquamating epithelial cells
-95%-97% is PMN, 60% of JE volume is due to that - Viable & non viable microorganisms |
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GCF electrolyte composition
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Na+/K+ proportion
K+ is released from dying cells Ca+ favors percipitation of glycoproteins (Inc calculus) |
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GCF Composition of organic compounds
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Carbs - glucose increases in Diabetes
Fibrinogen - Marker compound for inflammation Immunoglobulins & Complement Albumin Cytokines - IL1, IL8, others |
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GCF protease inhibitors
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a1-antitrypsin - Inhibits Elastase
a2-macroglobulin - Inhibits IL-2 |
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Inhibition of a1 Antitrypsin
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Oxygen radicals released by PMNs inhibits by oxydizing methionyl residue at active site
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GCF metabolic products
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Acids - Butyric & Propionic acids
Urea - NH4+ raises pH during inflammation as opposed to rest of body Bacterial antigens - LPS, LTA, N-formylated products Hydroxyproline - Collagen breakdown PGE & Arachidonic acid metabolites Pyridonoline telopeptide of type 1 collagen Osteocalcin Aspartate aminotransferase |
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GCF Enzymes
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Lysosomal Hydrolases - Cathepsins D for acid protease that breaks down epithelium for neutrophil migration
B is cystein protease same. Aryl sulfatase/b-glucuronidase Collagenase - MMP8-Neutrophils MMP1 - Fibroblasts Gelatinase - Type 4 collagenase MMP 9 - PMN MMP 2 -fibroblasts Elastase - Inhibited by a1-antitrypsin |
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Alpha 1 - Antitrypsin
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-Autosomal codominance inheritance with two single alleles
Pi MM normal Pi ZZ 15% of normal Pi SZ 35% of normal Pi SS 60% of normal |
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Commercial tests
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Periocheck - Collagenase
Periogard - aspartate aminotransferase Periostick - Cathepsins & neutral proteases |
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GCF clinical aspects
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-Directly related to inflammation (Gingivitis)
-Related to PD & bone regeneration (Osteocalcin) -Circadian periodicity -Hormonal effects -PMN chemotaxis assay -Source of antibiotics (tetracyclin concentrated) |
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Microbial aspects in the pathogenesis of PD (4)
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-A Specific clone of pathogenic subtype must be present in sufficient quanitity to initiate disease
-Must be able to colonize & grow -Able to avoid host defenses -Can secrete substances that directly initiate tissue destruction |
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3 examples of bacterial virulence factors
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-A actinomycetemcomicans & C rectus secrets leukotoxins that kill neutrophils
-P gingivalis produce proteolytic enzymes to destroy antibodies & complement -AA secrets factors that supress immune response |
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3 ways bacteria work
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- Organisms with fibriae or molecules such as adhesins can associate with tissues & other bacteria
-P gingivalis has a capsular polysaccharide that is resistant to host defense & complement -AA & P gingivalis can invade & preside in epithelial cells. |
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Bacterial virulence factors
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Antigens
Lipopolysaccharide (gram neg) Lipoteichoic acid (Gram pos) Enzymes (Collagenase Inhibitors Chemotactic factors (N-FMLP) Adjuvants Toxic motabolites (Butyric acid) |
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Properties of Lipoteichoic Acid
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-Adheres to dental surfaces
-Stimulates bone resorption -Anticomplement |
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Properties of Lipopolysaccharides
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B Cell mitogen
Activates complement anternative Mediates bone resorption Free LPS vesicles contain destructive enzymes Stimulates neutrophil enzyme release Generation of chemotactic factors T cell independent antigen |
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Direct effects of bacteria (4)
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-Alters gingival environment by toxic or proinflammatory by products & allow pathogens associated with PD to colonize & grow
-P. Ging produce enzymes to degrade -P. Ging produce by products H2S and NH3, & fatty acids that are toxic to cells -LPS stimulates bone resorption |
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Indirect effects of bacteria (3)
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-PMNs release enzymes that degrade host tissues
-Bacterial LPS can stimulate catabolic cytokines & Inflammatory mediators -Cytokines & Inflammatory mediators then stimulate release of MMPs |
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How are neutrophils attracted to the site of infection?
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-Complement C5a
-Microbial chemotactic factors N formylated peptides -Cytokines IL8 |
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Neutrophil function
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-Phagocytosis
-Lysosomal Enzyme release a. C5 cleavage -chemotactic b. Kinin generation - vasoactive peptides c. Superoxides - oxidative antimicrobial activity d. cationic proteins - lysozyme e. prostaglandins & thromboxanes f. Neutral proteases g. MMP 8, 9 |
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Disorders of PMN migration
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- Decreased locomotor capabilities
- Lowered response to chemotactic factors - Inhibitors of chemotaxis present |
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Shifts of lymphocyte populations
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T cell - Gingivitis
B/plasma cells - Periodontitis |
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Regulatory role of PMNs in PD
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Produces cytokines IL1 & cytokine inhibitors IL-1ra
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T memory cell phenotypic markers
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CD29 & CD45RA. Mediates B cell response
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Functional classification of T cells based on cytokine
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TH1 CD4 - IL2, IFNg - DTH, B cell supression
CD8 - IL2, IFNg - Toxic, B cell supression TH2 - IL4, IL10 - B cell help, DTH supression CD8 - IL4, IL10 - DTH supression, B cell help |
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TNFa (4)
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-Proinflammatory
-Release of MMPs -Eicosanoid production -Bone Resorption |
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IL1 (5)
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-Bone resorption
-Enables ingress of inflammatory cells -Eicosanoids -MMPs -ILa is predominant but ILb is 15x more powerful |
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IL6 (4)
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-Plasma cell proliferaion & antibodies
-Elevated in GCF of refractory PD -Stimulates osteoclasts -Produced by lymphocytes monocytes & fibroblasts |
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IL8 (4)
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-Chemoattractant for Neutrophils
-Stimulates nutrophils to release MMPs -Higher in GCF of PD - Produced by monocytes in response to LPS, IL1, TNFa |
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PGE2
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-Stimulates Bone resorption
-MMPs -Produced by monocytes & fibroiblasts |
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Antiinflammatory mediators
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TGF-b
IL-1ra IL-10 IL-4 TIMPs |
