Perio Exam 1 (second set of lectures)

D1 Fall

Risk Factors

tobacco smoking, diabetes, pathogenic bacteria and microbial tooth deposits

Risk Determinants/ Background Characteristics

genetic factors, age, gender, socioeconomic status, and stress

Risk Indicators

HIV/ AIDS, osteoporosis, infrequent dental visits

Risk Markers/ Predictors 

previous history of periodontal disease, bleeding on probing

What is risk assessment?

disease risk is the probability that an individual will develop a specific disease in a given period; determined by numerous components

Risk Factors for Periodontitis

may be environmental, behavioral, or biologic

How are risk factors identified?

by longitudinal studies of patients with the disease of interest 

to be considered a risk factor

exposure must occur before the onset of disease

exposure can occur at

single point, over multiple points, or continuous

Intervention

can help modify risk factors

contains more than 60 known carcinogens

tobacco smoke

associated with multiple diseases that reduce life expectancy and quality of life

smoking

Nicotine

highly addictive

Smoking

a major risk factor for periodontitis and affects the prevalence, extent, and severity of disease

what percent of periodontitis cases in US were current smokers

42%

what percent of periodontitis cases in US were former smokers

11%

current smokers are ___ more likely to have severe periodontitis compared to non-smokers

3x

relationship between smoking and prevalence and severity of periodontitis

dose-response

effect of smoking on gingivitis and periodontitis

negative effects of smoking on host are reversible, formers smokers respond to periodontal therapy similarly to non-smokers; to decrease risk for periodontitis a patient must increase number of years since quitting smoking 

periodontal disease effects of smoking: gingivitis

gingival inflammation and bleeding on probing

periodontal disease effects of smoking: periodontitis

prevalence and severity of periodontal destruction, pocket depth/ attachment loss/ bone loss, rate of periodontal destruction, tooth loss

effects of smoking on the etiology and pathogenesis of periodontitis: microbiology

increased complexity of microbiome and colonization of periodontal pockets by periodontal pathogens

effects of smoking on the etiology and pathogenesis of periodontitis: immune-inflammatory response

altered neutrophil chemotaxis, phagocytosis and oxidative burst; increase tumor necrosis factor-a and prostaglandin E2 in gingival crevicular fluid, increased neutrophil collagenase and elastase in gingival crevicular fluid, increased production of prostaglandin E2 by monocytes in response to lipopolysaccharide

effects of smoking on the etiology and pathogenesis of periodontitis: physiology

decreased gingival blood vessels with inflammation, decreased gingival crevicular fluid flow and bleeding on probing, decreased subgingival temperature, increased time needed to recover from local anesthesia

battery powered device that produces aerosol that is inhaled 

E-cigarettes

E-liquid contains

nicotine, dilutants, and flavorings

studies support that the use of e-cigarettes are unlikely to exceed ___ of the harm from smoking

5%

treating tobacco dependency

5As (Ask, Advise, Assess, Assist, Arrange)

Ask

discuss the patient’s smoking status

Advise

educate smokers of the associations between oral disease and smoking

Assess

gauge the patient’s interest to attempt to quit

Assist

help the patient in their attempt to quit smoking

Arrange

treatment plan referral or follow-up visit

Diabetes

metabolic disorder characterized by chronic hyperglycemia

periodontitis risk factor: diabetes

direct relationship, no difference between type I and type II, periodontal disease is 6th complication of diabetes

poorly controlled diabetics

altered immune function (PMNs), qualitative changes in bacteria, altered collagen structure and function, severe gingival inflammation, deep pockets, rapid bone loss, periodontal abscesses

poor response to therapy relative to well-controlled and non-diabetics

uncontrolled diabetics

5-fold increased prevalence in teenagers with type I diabetes

periodontitis

poorly controlled adult diabetic ___ times higher periodontitis prevalence

2.9

smokers with poorly controlled diabetes ___ times higher periodontitis prevalence

4.6

anatomic factors that harbor bacterial plaque

furcation, root concavities, grooves, cervical enamel projections, enamel pearls, overhanging margins, calculus

risk factor: non-modifiable

age, gender, genetic factors, stress, socioeconomic status

Genetic factors of periodontitis

alterations in neutrophils, monocytic hyperresponsiveness associated with serve periodontitis; alterations in IL-1 genes are one of several involved in periodontitis

Age factors of periodontitis

prevalence and severity increase with age, degenerative changes related to aging process, prolonged exposure to other risks over life lead to cumulative destruction, young individuals with periodontal disease are at greater risk for continued disease

Gender factors of periodontitis

men have more attachment loss than women, men have higher levels of plaque and calculus, gender differences in prevalence and severity appear to be related to preventive practice vs genetic

Socioeconomic status factors of periodontitis

gingivitis and poor oral hygiene related to lower SES, decreased dental awareness and decreased frequency of dental visits, SES alone does not result in an increased risk

Stress factors of periodontitis

emotional stress may interfere with normal immune function, stressful events lead to greater prevalence of periodontal disease, increase incidence of necrotizing ulcerative gingivitis during periods of high stress

Risk Indicator: HIV/ IADS

higher risk for periodontitis, higher degree of immunosuppression in adults w/ AIDS, increased periodontal pocket formation and loss of attachment, oral lesions prominent diagnostic feature

oral and periodontal manifestations of HIV infection

oral candidiasis, linear gingival erythema, oral hairy leukoplakia, Kaposi Sarcoma and other malignancies, acute necrotizing ulcerative gingivitis (ANUG), necrotizing ulcerative gingivitis and periodontitis, chronic periodontitis

Risk Indicator: Osteoporosis

does not initiate periodontitis, reduced bone mass aggravates periodontal disease progression, studies are conflicting but there may be a link

Risk Indicator: Infrequent Dental Visits

increased risk for severs periodontitis in patients who had not visits the dentist for 3 years or more

severe existing loss of attachment

predictor of future loss of attachment

no attachment loss 

a predictor for decreased risk for future loss of attachment

%BOP sites has a liner relationship with probing force

in healthy subjects

reason for BOP in absence of disease

tissue trauma

colonization of the oral cavity: Day 1 

starts at birth with facultative and aerobic

colonization of the oral cavity: Day 2

anaerobic bacteria can be detected

colonization of the oral cavity: Day 14

by two weeks mature microbiota is established in gut of newborn

colonization of the oral cavity: Age 2

human microbiota is formed, by this time 10^14 microorganisms populate the body

After tooth erruption

more complex oral flora; most are commensal and beneficial

6 Major Ecosystems in Oral Cavity

buccal mucosa, gingiva, palate, dorsum of tongue, intraoral/ supragingival/ hard surfaces, subgingival biofilm

differentiated from materia alba and calculus

plaque

Dental Plaque

a structured, resilient, yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restorations

supragingival plaque

located above the gumline

subgingival plaque 

below the gumline

Materia Alba

white, cheeselike accumulation; lacks an organized structure and is therefore not as complex as dental plaque

easily displaced with a water spray

Materia Alba

Dental Plaque

resilient clear to yellow-grayish substance; considered to be a biofilm

impossible to remove by rinsing or with the use of sprays

dental plaque

Calculus

hard deposit that forms via the mineralization of dental plaque; generally covered by a layer of unmineralized dental plaque

Materia Alba (MA)

soft accumulation of salivary proteins, some bacteria, many desquamated epithelial cells, and occasional disintegrating food debris

Dental Plaque (DP)

primarily composed of bacteria in a matrix of salivary glycoproteins and extracellular polysaccharides

3 major phases of plaque formation 

1. formation of pellicle on tooth surface 2. initial adhesion and attachment of bacteria 3. colonization and plaque maturation 

Dental Pellicle

all surface of oral cavity coated; consists of glycoproteins, proline-rich proteins, phosphoproteins, histidine-rich proteins, enzymes (adhesion sites for bacteria), mechanism of formation are hydrophobic forces (van der Waals)

within nanoseconds after polishing teeth, they are covered with saliva-derived layer

derived pellicle

Initial Adhesion and Attachment of Bacteria: Phase 1

transport to surface/ random contact

Initial Adhesion and Attachment of Bacteria: Phase 2

initial adhesion - reversible

Initial Adhesion and Attachment of Bacteria: Phase 3

attachment - form anchorage; depends on specific interactions between microbial cell adhesin molecules and receptors in pellicle

disappear after full mouth extractions

key periodontal pathogens

Teeth and Implants

hard, non-shedding surface that allows development of extensive structured bacterial deposits

“port of entry” for peripathogens

teeth

supragingival plaque in contact with gingival margin

marginal plaque

supragingival plaque bacterial composition at tooth surface

gram positive cocci and short rods predominate

supragingival plaque bacterial composition at outer surface

gram negative rods, filaments, spirochetes

topography of supragingival plaque

initial growth along gingival margin and interdental space; forms along grooves, crack, pits, and fissures; further extension in coronal direction

factors affecting supragingival dental plaque formation

rough surfaces accumulate and retain more plaque, thicker plaque is more pathogenic with more mobile organisms

decreases rate of plaque formation 

smoothing surfaces 

plaque formation within dentition

forms faster in lower jaws, molar areas, and buccal/ interproximal surfaces

individual variable influencing plaque formation

rate of formation, saliva-induced aggregation (salivary flow conditions explain 90% of variation), diet, smoking, tongue/ palate brushing antimicrobial factors in saliva

does age influence de novo plaque formation?

NO

is plaque removed spontaneously during eating?

NO

plaque forms faster adjacent to

inflamed gingiva 

subgingival plaque

differs due to availability of blood products and anerobic environment

difficult to remove

subgingival plaque

subgingival plaque formation 

bacteria are source for recolonization, some pathogens penetrate soft tissue and dentinal tubules, fast re-growth to pre-treatment level within 7days

tooth associated subgingival plaque

cervical plaque similar to supragingival plaque, deeper parts of pocket (less filamentous), apical portion dominated by smaller organisms without particular orientation

tissue associated subgingival plaque

contain primarily gram-negative rods and cocci, large number of filaments, flagellated rods, and spirochetes

plaque as a biofilm

have organized structure, in lower layers bound together by polysaccharide matrix and organic/ inorganic materials, nutrients run through fluid channels in plaque mass

plaque as a biofilm: quorum sensing

how bacterial cells communicate with each other

transmissible

periodontal pathogens and cariogenic bacteria