Perio Risk Factors Lecture 3

Define risk in the context of periodontal disease.

The probability that an individual will develop a specific disease within a given period, influenced by environmental, behavioral, and biological factors.

Differentiate between risk factor, determinant, indicator, and marker.

Risk Factor: Causal, from longitudinal studies (e.g., smoking, diabetes, bacteria).
Risk Determinant: Non-modifiable traits (e.g., age, gender, genetics, SES, stress).
Risk Indicator: Probable factor from cross-sectional studies (e.g., HIV/AIDS, osteoporosis, infrequent dental visits).
Risk Marker/Predictor: Associated with disease but not causal (e.g., past periodontitis, BOP).

List the three primary risk factors for periodontitis.

Tobacco smoking, Diabetes mellitus, and Pathogenic bacteria in dental biofilm.

What criteria must be met for an exposure to be considered a true risk factor?

Exposure must precede disease onset and be supported by longitudinal data; modifying the exposure reduces disease risk.

How does smoking influence periodontitis prevalence and severity?

42% of US cases are current smokers, 11% former smokers. Current smokers have ~3× higher risk for severe periodontitis. Shows dose-response with severity.

Describe the pathophysiologic effects of smoking on the periodontium.

Impaired neutrophil and fibroblast function, altered cytokine expression, reduced vascularity, enhanced biofilm virulence.

Are smoking effects reversible?

Yes. Former smokers respond to therapy similarly to non-smokers; risk decreases with years since quitting.

Outline the 5 A’s of smoking cessation counseling.

Ask, Advise, Assess, Assist, Arrange.

What is the evidence for e-cigarettes relative to tobacco smoking?

2021 Cochrane Review: effective for cessation and likely ≤5% of the harm of smoking; not risk-free.

Summarize the relationship between diabetes and periodontitis.

Direct, bidirectional relationship. Periodontitis is the 6th complication of diabetes; hyperglycemia worsens immune response, collagen metabolism, and healing.

How does poor glycemic control affect periodontal outcomes?

Altered PMN function, qualitative microbial changes, defective collagen metabolism → severe inflammation, deep pockets, rapid bone loss, abscesses.

Compare prevalence by diabetic control and smoking status.

Type 1 teen diabetics: ~5× higher; poorly controlled adults: ~2.9× higher; smokers with uncontrolled DM: ~4.6× higher odds.

How do uncontrolled diabetics respond to periodontal therapy?

Significantly poorer healing and less attachment gain than well-controlled or non-diabetics.

Why is biofilm quality more important than quantity?

Certain pathogens (A. actinomycetemcomitans, P. gingivalis, T. forsythia) drive progression regardless of total plaque amount.

What anatomic factors favor plaque retention?

Furcations, root concavities, grooves, cervical enamel projections, enamel pearls, overhanging restorations, calculus.

Which determinants are non-modifiable but influence risk?

Age, Gender, Socioeconomic status, Genetics, Stress.

How does age affect periodontitis risk?

Prevalence/severity increase with age due to cumulative exposure; young patients with disease have higher future risk.

Explain gender differences in periodontitis.

Men show more attachment loss and plaque; differences largely due to preventive habits rather than biology.

Describe the impact of socioeconomic status.

Lower SES → more gingivitis and poorer hygiene due to limited awareness and dental access; SES alone not causal.

How does stress influence periodontal disease?

Chronic stress impairs immune function and increases NUG/periodontitis prevalence.

What genetic factors are linked to periodontitis?

IL-1 gene polymorphisms, neutrophil dysfunction, monocytic hyperresponsiveness, twin studies confirm heritability.

Define risk indicator and list examples.

Probable risk factor from cross-sectional studies: HIV/AIDS, osteoporosis, infrequent dental visits.

How does HIV/AIDS alter periodontal presentation?

Greater immunosuppression → more attachment loss and pocketing; oral lesions assist in diagnosis.

List common oral manifestations of HIV infection.

Candidiasis, linear gingival erythema, hairy leukoplakia, Kaposi sarcoma, ANUG/NUP, chronic periodontitis.

What is the relationship between osteoporosis and periodontitis?

Does not initiate disease but may exacerbate progression; low bone mass linked to attachment loss.

How do infrequent dental visits act as a risk indicator?

≥3 years without visits → greater severity; ≥6 years without care not necessarily associated with increased progression.

What are the two most important clinical risk markers for future disease?

Past periodontitis history and bleeding on probing (BOP).

Why is prior attachment loss significant?

Existing loss predicts future loss; absence predicts stability.

Interpret bleeding on probing (BOP) as a predictive measure.

Frequent BOP → low PPV (~6%); absence → high NPV (~98%) for stability; continuous absence indicates health.

How are risk factors incorporated into clinical assessment?

Smoking: cessation; Diabetes: monitor A1C; Microbes: sampling/testing; Genetics: IL-1 test; Age/Gender/SES/Stress: tailor recall and education.

Summarize the main conclusion of the lecture.

Risk assessment identifies factors predisposing/modifying disease; patient education and targeted interventions improve outcomes.