Perio Exam 2

What is a biofilm?

-bacteria attached to a surface embedded in a extracellular matrix formed by DNA, proteins, and polysaccharides -bacteria live in community known as biofilm -biofilm bacteria are often up to 1000 times more resistant to antimicrobial agents (antibiotics) than their planktonic (free-floating) counterparts free floating are more likely to be susceptible to antibiotics

Subgingival plaque

-below gingival margin -bathed with gingival crevicular fluid (GCF) -filamentous predominance and in deeper pockets a decrease in filamentous -anerobic environment -availability of blood products (why black) -apical: spirochetes, rods, cocci -can have bacteria in the tissue which can directly or indirectly resorb bone

How does bacteria invade the gingival connective tissue?

-NUG: bacteria actually in CT punched out papilla, spontaneous bleeding, pain bc NUG is an abcess -Chronic advanced periodontitis aka stage 3/ severe periodontitis -Localized aggressive periodontitis: AA in the tissue

What are the predominant inflammatory cell in crevicular fluid? What about CT?

-PMN/ neutrophil 1st cell in inflammatory response actute inflammatory response helps in minimizing the effects of bacteria -in connective tissue the predominant cell is plasma cell in periodontitis

What is localized aggressive periodontitis?

-aka molar/incisor pattern, stage 3, grade C -75% of LAP patients exhibit a neutrophil chemotactic defect (neutrophil cant get to site of inflammation) -Associated with A. actinomycetemcomitans -increased antibody level to A. actinomycetemcomitans are found in serum, GCF and saliva

There is a positive correlation bw the ______ of GCF and/or some of its components and the _______ of gingival inflammation

-amount (what is measured on a periotron) -severity

How long has periodontitis been around?

-anthropologic evidence suggests that severe periodontal disease was present in our ancestors

Prevalence of Periodontal Disease

-anthropologic evidence suggests that severe periodontal disease was present in our ancestors -severity decreasing in industrialized nations: as health care improves and awareness increases -prevalence of gingivitis in US children 5-17 years was 95%. 28% had half or more teeth affected

Xerostomia

-associated with an increase in inflammatory gingival diseases and a higher incidence of dental carries

Supragingival plaque

-at or above gingival margin -gram positive cocci are short rods predominate at the tooth surface -gram negative rods, filaments and spirochete predominate in the outer surface of the mature plaque mass

Relative risk (smokers relative to non-smokers): trends

-attachment loss: increases with increase dose of smoking -bone loss: for a heavy smoker, there is a 7x greater risk of bone loss

What is the role of saliva in the oral health?

-lubrication -physical protection: glycoproteins, mucoids -cleansing: physical flow -buffering: biocarbonate and phosphate, reduce carries by neutralizing pH -tooth integrity maintenance bc minerals in saliva and glycoprotein pellicle -antibacterial action: IgA: control of bacterial colonization; lysozyme: breaks bacterial cell walls; lactoperoxidase: oxidation of susceptible bacteria

Pathways to periodontal disease: genetic risk factors

-male gender -race: hispanics, african american -diabetes -down syndrome -rare genetic diseases

NIDR: Mean attachment loss statistics (18-64 yrs old)

-males: 2.04mm -females: 1.80 mm

indices for plaque and debris: turesky modification of the quigley-hein index

-measures the surface area of plaque on the tooth -0= no plaque -1= separate flecks of plaque at the cervical margin of the tooth -2= thin continuous band of plaque (up to 1 mm) at the cervical margin -3= band of plaque thicker than 1 mm but covering less than 1/3 of the crown -4= plaque covering 2/3 or more of the crown

indices for plaque and debris: plaque index (silness and loe) *test question

-measures thickness of plaque at the gingival margin -0= no plaque in the gingival area -1= A thin film of plaque at the gingival margin. visible only with explorer -2= moderate accumulation of plaque at the gingival margin. Plaque VISIBLE with naked eye -3= thick, abundant, visible plaque at the gingival margin

What are the potential roles of prostaglandins in inflammation? *test

-mediate vasodilation -act synergistically with histamine and bradykinin to increase vascular permeability -modulate T lymphocyte functions including inhibition of cytokine production -stimulate osteoclastic bone resorption** test

How do microorganisms cause periodontitis both indirectly and directly?

-micro-organisms may cause periodontitis indirectly by stimulating a host response (macrophages, neutrophils) or directly via the production of bacterial toxins

What are the potential biological functions of complement: C3b?

induction of macrophage secretion and cytokine production, opsonization (coat bacteria so macrophages can recognize) of micro-organisms for phagocytosis, stimulation of leukocyte oxidative metabolism

Periodontitis

irreversible inflammation of the periodontium (including PDL and alveolar bone) -chronic disease we do not cure just manage -gingival inflammation (in common with gingivitis) -periodontal pockets (not psuedopockets) -attachment loss -bone loss -tooth mobility (possibly)

What are the potential biological functions of complement: C5a?

leukocyte chemotaxis, stimulation of leukocyte oxidative metabolism, activation of neutrophil and mast cell degranulation, increases vascular permeability (C3a also increases vascular permeability through histamine)

What is an exotoxin example?

leukotoxin -part of invasion of host response -produced by AA, toxic to WBC like PMNs, monocytes and leukocytes

What are the bacterial and host factors that can play a role in bone resorption? *test

*bacterial factors that can induce bone resorption -LPS (bacterial product) -Lipoteichoic acids (gram positive) and muramyl dipeptides (gram positive and gram negative organisms) (part of the peptidoglycan of bacteria and certain fragment is associated with bone resorption) *host factors that can induce bone resorption -PGE2- produced by host as fatty acid -IL-IB -TNFa and TNFB -IL-6

What are the factors that stimulate in vitro bone resorption?

*bacterial factors that can induce bone resorption -LPS (bacterial product) -Lipoteichoic acids (gram positive) and muramyl dipeptides (gram positive and gram negative organisms) (part of the peptidoglycan of bacteria and certain fragment is associated with bone resorption) *host factors that can induce bone resorption -PGE2- produced by host as fatty acid -IL-IB -TNFa and TNFB -IL-6

indices for plaque and debris: gingival index (loe and silness) *test question

-0= normal gingiva, no inflammation, no bleeding -1= mild inflammation, slight change in color (redness), slight edema, NO BOP -2= moderate inflammation, redness (erythema), edema, BOP -3= severe inflammation, marked redness (erythema) and some ulceration, TENDENCY TO BLEED SPONTANEOUSLY

NIDR: gingival bleeding statistics (18-64 yrs old)

-50% in males, 39% in females -females better clinical presentation, better hygiene?

NIDR: site with at least 4 mm attachment loss (18-64 yrs old)

-75% had at least 1 site with 4 mm attachment loss

What is the hypothetical model for acute burst of disease activity?

-Aggregatibacter actinomycetemcomitans colonize the sulcus -Leukotoxin secreted by this organism may destroy PMNs and macrophages, resulting in an impairment of the host response -disintegration of killed PMNs results in the release of lysosomal products into the surrounding tissues -damage to CT occurs -an immunosuppressive factor produced by A. actinomycetemcomitans activates T suppressor cells -this localized immunosuppression may allow periodontal pathogens to proliferate within the sulcus and, perhaps, even invade the underlying CT

What is the predominant immunoglobulin in saliva? What about in crevicular fluid?

-IgA in saliva -IgG in crevicular fluid

What is the composition of GCF?

-cellular elements: bacteria (bc going subgingivally), desquamated (sluffed off from sulcular or junctional epithelium) epithelial cells, **PMNs (predominantly), mononuclear cells -Electrolytes: K+, Na+, Ca++ -organic compounds: glucose, immunoglobulins (IgG predominantly (IgA in saliva), complex fragments -bacterial products: LPS (endotoxin, gram negative bacteria) -enzymes: B-glucuronidase, lactic acid dehydrogenase, alkaline phosphatase, lysozyme derived from host cells (derived from host cells) -metabolic products: lactic acid, urea and hydrogen sulfide (products of bacteria that end up in the crevicular fluid) -mediators of inflammation (cytokines: IL-1, TNFa, Prostaglandin E2, fatty acid)

What is a periodontal lesion?

-characterized by loss of alveolar bone -plasma cells still predominate in CT -pocket formation -periods of destruction followed by periods of remission (cyclical pattern of destruction) -irreversible

Periodontitis

-chronic inflammatory disease: it is chronic, do not cure just manage -host-bacterial (subgingival biofilm) interactions determine the nature and extent of the disease -not everyone dev periodontits (42%) -micro-organisms may cause periodontitis indirectly by stimulating a host response (macrophages, neutrophils) or directly via the production of bacterial toxins

What are the factors affecting GCF flow?

-circadian periodicity: gradual increase in the amount of GCF from 6am to 10pm and dec over night increase in volume throughout the day (similar to saliva), why use prescription fluoride before bed -sex hormones: (female hormones) increase vascular permeability, increase inflammation, increase GCF ex: puberty, pregnancy -mechanical stimulation: chewing inc flow, transient -periodontal therapy

Classical vs alternative pathway of activation *test

-classical: activated by antibody antigen complexes -alternative: activated by LPS endotoxin

What is the antibacterial action of GCF/ properties of GCF that enable it to play a protective role?

-cleansing action: continuous flow from the base of the pocket coronally and it flushes out the pocket -antibacterial properties ex: IgG, lysozymes: host enzyme that breaks bacterial cell walls -adhesive properties: allow junctional epithelium to adhere to tooth so don't get apical migration of attachment apparatus it plays a protective role for the host

What are the representative products secreted by activated macrophages?

-collagenase, elastase -complement components -lysozyme -cytokines: all bone resorbing cytokines IL-1, IL-6 and TNFa -Prostaglandin E2 (fatty acid, also associated with bone resorption) and other eicosanoids reduce in PGE2 when take NSAID for fever -fibroblast and endothelial cell mitogens (involved in wound repair)

Cytokines

-cytokines are protein intracellular messengers; intracellular molecules that mediate interactions bw cells this is the old classification -MIF (macrophage migration inhibition factor= now likely IL-4) -MAF (macrophage activation factor= INFy) -OAF (osteoclast activating factor= IL-1B and IL-6) -Lymphotoxin (now called TNF-B)

Structure of a mature dental plaque biofilm

-dental plaque: primarily composed of bacteria in matrix of salivary glycoproteins and extracellular polysaccharides considered to be a biofilm impossible to remove by rinsing or with the use of sprays -one gram of plaque contains 10^11 bacteria. In a periodontal pocket, bacteria counts can range from 10^3 in a healthy crevice to 10^8 in a deep pocket -calculus: hard deposit that forms via the mineralization of dental plaque generally covered by a layer of unmineralized dental plaque plaque harbors calculus which is why we remove it

How does the bacteria evade the host response?

-destruction of PMNs (A. actinomycetemcomitans leukotoxin) -Inhibition of PMN chemotaxis (capnocytophaga) -impairment of PMN adherence and phagocytosis (polysaccharide capsule of black pigmented Bacteroides, now called P. gingivalis) -inhibiton of oxygen radical activity (superoxide dismutase and catalase of P. gingivalis and A. actinomycetemcomitans) -degradation of lactoferrin (P. gingivalis) -IgA, IgG and IgM proteases: degrade immunoglobulin -C3 and C5 proteases: degrade complement -activation of T suppressor cells: immunosuppressive response (A. actinomycetemcomitans)

What are the potential roles of neutral proteases in inflammation?

-destruction of connective tissue components: collateral damage -digestion of gram-positive and gram-negative bacteria -digestion of immunoglobulins: want immune response to stop at some point -activation of alternate (activated by LPS endotoxin) complement pathway -generation of kinins (vasoactive) -stimulation of B lymphocyte proliferation and antibody production)

Public health perspective vs private practitioner perspective

-diff patient population -diff satisfaction

What is linear gingival erythema (formerly HIV-gingivitis)?

-distinct form of gingival inflammation -characterized by fiery red gingiva and edema in the attached gingiva which may extend beyond the mucogingival jxn

What does periodontits result from?

-inadequate or excessive host response, the presence of virulent microorganisms or a combination of the two -the host response may be both protective and destructive

What are the causes of Xerostomia?

-drugs: anti-hypertension (blood pressure meds), antidepressants, anti-anxiety, antipsychotics, antihistamine and deconjustants -radiation therapy of head and neck or chemotherapy -mouth breating: max anterior gingiva -Scrojens syndrome: autoimmune disease -smokers -age -alcohol use -meth use -stress Symptoms -gloves stick to mouth -sensitivity/ discomfort -fissure of tongue -redness -hard to chew, speak, swallow -altered sensation of taste -harder to wear dentures -bad breath (also caused by NUG, periodontitis, bacteria on tongue, foods, sinus drainage, poor oral hygiene) Treatment -biotene toothpaste, xyoitol, drink water, chew sugarless gum, prevident 5000, act mouthwash (0.05 fluoride rinse)

Colonization of the oral cavity

-early on many streptococci -also early on have staph, which is not usually present in the oral cavity and it diminishes over time

What are the cell constituents?

-endotoxin (LPS): can stimulate bone resorption, activate alternate complement cascade, stimulate macrophage to release biologically active molecules like bone resorbing cytokines -peptidoglycan: can cause bone resorption, component of bacteria -toxin end products of metabolism (ammonia, H2S, and butyric acid): bacteria have own toxic products

2009-2014 NHANES Survey: periodontitis stats

-estimates derived from a sample of 11,753 adults aged 30+ with one or more natural teeth -full mouth periodontal examination (3rd molars excluded) unlike NHANES III -42% of dentate adults age 30+ had periodontitis -7.8% of individuals age 30+ had severe periodontitis -59.8% of adults age 65+ had periodontitis -highest among men (50.2%), current smokers (62.4%), and those with self-reported diabetes (59.9%) -highest among Mexican Americans (59.7%) and adults below 100% federal poverty level (60.4%)

T/F There is an inflammatory mediator that predicts future disease activity There is an inflammatory mediator or other GCF component that is predictive of future attachment loss (ie progressive periodontitis)

-false, there is no mediator that predicts disease activity -so you have to measure the pocket at every visit and see if there is any change

How is GCF collected?

-filter paper strips (primarily used) isolate the area bc don't want saliva, place strip subgingivally until meets some resistance -microcapillary pipets -periotron= measure of GCF

Pathways to periodontal disease

-genetic risk factors -tissue breakdown products and ecological factors -environmental and acquired risk factors

History of periodontal disease: traditional concept of disease progression

-gingivitis --> periodontitis -slow, continuous progression these are disproved

When should you use antibiotic prophylaxis?

-heart valve so it doesn't lead to infective endocarditis -don't need for joint infections -do w immunocompromised -don't need to do if controlled diabetes

The oral cavity from a microbe's perspective

-human fetus is sterile -within hours, oral cavity is colonized by low numbers of mainly facultative (can survive in either aerobic or anerobic env) and aerobic bacteria -within 2 weeks, the microbiota in the gut is mature -after 2 years, the entire human microbiota is formed. The body contains 1.3 to 10 times more bacteria than human cells -after tooth eruption, a more complex microbiota forms in the mouth -it is estimated that the oral cavity houses approximately 700 different species, approximately half of which can be present at any time in any individual -most oral bacteria are harmless commensals (live in harmony with the host); fewer are pathogenic

What are the enzymes present?

-hyaluronidase -bacterial collagenase -phospholipase A= bone resorbing fatty acid (release arachadonic acid, precursor for PGE2, NSAID blocking this), gelatinases, acid and alkaline phosphatases

What are the protective aspects of host response?

-immunoglobulins found in gingival crevicular fluid (IgG) can inhibit colonization and adherence of bacteria to oral surfaces -neutrophils and macrophages, by phagocytosis, can reduce bacterial load -salivary lysosome (degrades bacterial cell walls), lactoperoxidase (oxidize susceptible bacteria), lactoferrin (bind iron) and sIgA function in supragingival environment and help prevent extension of plaque into sulcus

What are the potential functions of PMN oxygen radicals in inflammation?

-microbiocidal -cause damage to surrounding host cells -cause depolymerization of structural matrix of tissues -inactivate chemotactic factors: C5a that induces leukocyte chemotaxis -they can kill bacteria but in doing so they will also damage host cell and CT

Overview on periodontal studies

-most populations in industrialized countries have gingivitis -periodontitis prevalence is lower than gingivitis -periodontitis is an important public health problem -however, a small percentage (8-15%) of the population is at risk for severe periodontitis -severity of disease increases with age -bottom line: edentulism is decreasing in the US

What are the neutrophil disorders associated with periodontitis?

-need a good host response -cyclic neutropenia: significant dec in PMN for a 4-5 day period and then comes back to normal neutrophil level -drug-induced agranulocytosis: acetaminophen, penicillin, anticonvolsuants, NSAIDS -Chediak-Higashi syndrome: autosomal recessive disease with delayed neutrophil chemotaxis -Papillon-Lefevre syndrome: hyperkaratonosiss of palms of hands and soles of feet, lose teeth prematuraly -Down syndrome: trisomy 21, decreased PMN chemotaxis and phagocytosis -Leukocyte adhesion deficiency: manifestation of a systemic disease, neutrophils can't get from bloodstream to site of infection, there is a problem with migration and immigration of PMNs

What are the leukocytes in GCF?

-neutrophils/PMN predominate and are the first time of defense -phagocytic and killing capacity of neutrophils -protective deficiency in the numbers of neutrophils leads to a higher chance of periodontitis dev bc need the neutrophils there ex: neutrophenia is a dec in number of neutrophils and these patients have a greater risk for dev periodontitis also if neutrophils have a delayed chemotaxis-> greater risk for periodontitis

Epidemiology Prevalence

-number of events or defects in a population at one point in time ex: right now the prevalence of periodontitis is 42%

What does saliva contain?

-numerous antibacterial factors (immunoglobulins: predominantly IgA (IgG in crevicular fluid); also, lysozyme (break bacterial cell walls and also in crevicular fluid) and lactoperoxidase are present) -enzymes (amylase: digestive enzyme, hyaluronidase, B-glucuronidase, collagenase: degrades collagen) ex: collagen is the primary structural protein in body, it inhibits collagenase activity in periodontium and can stabilize periodontal disease progression collagenase in crevicular fluid is predominantly from host collagenase activity inc in periodontitis -Glycoproteins (helps form salivary pellicle), salivary buffers (why ppl w dry mouth at inc risk of carries), coagulation factors, desquamated epithelial cells and leukocytes

Pathways to periodontal disease: environmental and acquired risk factors

-oral hygiene in patients susceptible -medications: ca2+ channel blockers** (amlodipine= associated w ginigval overgrowth, Nifedipine, reapamil), dilantan (seizure med), cyclosporin -dry mouth: antihistamine, antidepressant, antianxiety, antipsychotic -smoking -HIV -vitamin, calcium and vit D -education -diabetes -smoking

What is the humoral immune response to plaque antigens?

-plaque antigens enter the CT via the junctional epithelium (from sulcus) -B-lymphocytes proliferate, develop into plasma cells and produce antibodies in response to the plaque antigens -antigen/antibody complexes are formed and activate the classical complement cascade -vascular permeability and leukocyte chemotaxis occur in response to complement cleavage products -neutrophils phagocytose the immune complexes and release inflammatory mediators into the surrounding tissues -macrophages also release inflammatory mediators which may promote tissue damage

What is the cell-mediated immune response to plaque antigens?

-plaque antigens penetrate into the CT -macrophages process the antigens and present them to T lymphocytes -the T lymphocytes proliferate and release cytokines: intracellular messengers that result in intracellular communication (IL-1, IL-6, TNFa) -cytokines may cause increased inflammation, tissue damage and bone resorption (release some collagenase to degrade collagen) -activated macrophages may also release inflammatory mediators

Risk factors for and indicators of periodontitis

-poor oral hygiene (risk factor only in susceptible host ex: smoker, diabetic, genetic risk factor) -tooth malposition (NOT considered a risk factor or indicator for periodontitis) -iatrogenic dentistry: more bone loss associated with overhanging restorations -smoking -nutrition (recent studies on calcium, vit D and vit C suggest relationship bw deficiencies and periodontitis) -advancing age -diabetes and other systemic diseases (RA, osteoporosis, AIDS, Papillon-Lefevre syndrome) -Male gender -race and ethnicity: black americans and mexican americans have higher periodontitis prevalence, but difference is likely due to socioeconomic factors -genetics

What is the clinical significance of GCF? *impt points

-positive correlation bw amount (what is measured on periatron) of GCF and/or some of its components and the severity of gingival inflammation -no inflammatory mediator or other GCF component is predictive of future attachment loss (ie progressive periodontitis)

What is the prevalence of gingivitis in children?

-prevalence of gingivitis in US children 5-17 years was 95%. 28% had half or more teeth affected

Use of antibiotics: tetracyclines

-reach a concentration in the GCF 2 to 10 times that in blood -doxycyclin, minocyclin -they concentrate in the crevicular fluid so the concentration here is much higher than in the bloodstream -generally conservative with prescribing but will use if see swelling, lymphadenopathy, fever, ect

What are the antibacterial factors produced by neutrophils (PMNs)?

-reactive oxygen metabolites (H2O2, -O2, OH*) -myeloperoxidase: can inhibit bacterial growth these two are part of the oxidative pathway: oxidation is toxic to pathogens -lysozyme: break down bacterial cell walls -lactoferrine: bind iron, iron is a nutrient for bacteria to grow -neutral proteases (fxn at pH 7.4=neutral) (elastase, collagenase, cathepsin G)

Gingival crevicular fluid (GCF) *test question

-serum EXUDATE -serum that exists subgingivally vs saliva that exists supragingivally -protein rich, high specific gravity, high vascular perm so high fluid; more inflammation= more vol -inflammatory exudate, more inflammation= more vol of fluid you have -doxycycline= antibiotic to inhibit collaganase activity and reduces bacteria counts

What is necrotizing ulcerative periodontitis (formerly HIV-periodontitis)?

-severe gingival inflammation -severe oral pain -rapid destruction of periodontal attachment -exposure of bone loss -spontaneous bleeding

NIDR: severity with age (18-64 yrs old) bleeding mean attachment loss

-severity increases with age a) bleeding: greater than 65 yr, retired males= 53% greater than 65 yr, retired females= 44% b) mean attachment loss: greater than 65 yr, 3.54 mm, males greater than 65 yr, 2.99 mm, females

Where is staphlyococcus aureus found?

-skin usually -not usually common in the mouth

What is generalized aggressive periodontitis?

-stage 3 grade C -P. gingivalis: the most prevalent organism -increased antibody levels to P. gingivalis found in serum, GCF and saliva -have neutrophil or monocyte chemotactic defects -high level of bone loss in young patients

Purpose of epidemiology

-study history of disease -diagnose community problems of health and disease -identify clinical syndromes -evaluate need and effectiveness of treatment -identify causes of health and disease

NHANES II: gingival bleeding and periodontitis stats not testing on bc too old

-subsample of 9,680 dentate adults 30 to 90 years of age received a periodontal examination (representative of 105.8 million civilian, institutionalized Americans) -50% of US adults had gingival bleeding -estimated that 35% of US adults have periodontitis

Putative periodontal pathogens: What makes up the orange complex bacteria?

-the bacteria are not enough to cause disease: need a susceptible host -also pathogenic bacteria but next tear -Fusobacterium nucleatum -Parvimonas micra -Prevotella intermedia -Prevotella nigrescens -Eubacterium nodatum -Campylobacter rectus

What are the 6 major ecosystems (niches) in the mouth?

-the intraoral, supragingival, hard surfaces (teeth, implants, restorations, and prostheses) -subgingival regions adjacent to a hard surface, including the periodontal/peri-implant pocket (with its crevicular fluid, the root cementum or implant surface, and the pocket epithelium) -the buccal epithelium, palatal epithelium, and the epithelium of the floor of the mouth -the dorsum of the tongue -the tonsils -the saliva

Putative periodontal pathogens

-the orange and red complex bacteria generally appear after the early colonizers are established. early colonizers include, for example, Streptococcus species, actinomyces species and Veillonella parvula -*Aggregatibacter actinomycetemcomitans is a periodontal pathogen (not a red or orange complex bacteria) associated with localized aggressive periodontitis

Epidemiology

-the study of the distribution and determinants of health related states or events (including disease), and the application of this study to the control of diseases and other health problems

indices for plaque and debris: o'leary plaque control record

-this is used in clinic -presence of plaque scored on four surfaces (mesial, distal, facial, lingual) -score= number of sites with plaque/ number of teeth x4 ex: 10 sites of plaque w 25 teeth x 4= 10% -goal of 20% or less (10% in dental hygiene clinic)

indices for plaque and debris: mobility: miller *test question

-two blunt instruments and measure mobility 0= no detectable movement 1= barely detectable movement 2= crown moves up to 1 mm in any direction 3= crown moves more than 1 mm in any direction or is depressible

What is the inflammatory response?

-vascular changes (vasodilation and increased blood flow) -biochemical mediators (histamine and serotonin increase vascular permeability) -cellular changes (leukocyte margination and emigration)

Accumulation of a dental plaque biofilm

1. formation of pellicle on tooth surface 2. initial adhesion/ attachment of bacteria to the pellicle/ glycoprotein 3. Colonization/ plaque maturation

Relative risk (smokers relative to non-smokers): moderate smoker

15.1-30 pack years -attachment loss: 2.77 -bone loss: 5.79

What is the threshold for localized vs generalized aggressive periodontitis?

30% or more of teeth involved

Relative risk (smokers relative to non-smokers): heavy smoker

30.1-150 pack years -attachment loss: 4.75 -bone loss: 7.28

In NHANES survey (2009-2014) what percentage of dentate adults age 30+ had periodontitis? test question

42% -7.8% had severe periodontitis -59.8% of 65+ -highest among men (50.2%), current smokers (62.4%), and those with self-reported diabetes (59.9%) -highest among Mexican Americans (59.7%) and adults below 100% federal poverty level (60.4%)

Relative risk (smokers relative to non-smokers): light smoker

5-15 pack years -attachment loss: 2.05 -bone loss: 3.25

What is the periodontal pathogen (not a red or orange complex bacteria) associated with localized aggressive periodontitis or molar incisor periodontitis? *test

Aggregatibacter actinomycetemcomitans

Putative periodontal pathogens: What makes up the red complex bacteria? *test

All culustered together, pathogenic bacteria that we see) -Porphyromonas gingivalis -Tannerella forsythia -Treponema denticola (spiroquite)

What complement proteins increase vascular permeability? *test

C3a and C5a

What are the bone resorbing cytokines? *test

IL-1, IL-6 and TNFa

Epidemiology Incidence

Number of defects (ex: new cases) that occur over a period of time ex: 1000 new cases last month

What is the predominant collagenase in crevicular fluid? *test

host collagenase -collagenase produced by patients own PMNs

What is a periotron?

measures GCF to measure volume of GCF

What are the potential biological functions of complement: C5b-9?

membrane attack complex- lysis of certain gram negative bacteria and destruction of host cells

History of periodontal disease: current concepts

random burst model (goodson 1982, Socransky 1984) -site specific: may not be generalized -brief destruction followed by remission: why probe pt every visit to keep pt stable

Gingivitis

reversible inflammation of the gingiva. Symptoms include bleeding, red and swollen gingiva

Is the severity of periodontitis increasing or decreasing over time?

severity decreasing in industrialized nations: as health care improves and awareness increases