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public health of perio disease (Public health approach: define health…
public health of perio disease
Public health approach: define health problem, risk factors, test com-level interventions to control cause, interventions to improve health of pop, monitor, assess effectiveness
Health problem: chronic periodontitis – chronic inflam response in reaction to toxins by bacteria in biofilm in which body turns upon itself & support tissues for teeth destroyed, accompanied by loss of attachment of tissues, progression of attachment loss slow but rapid progression can occur
Risk factors: precedes disease outcome (smoking), risk indicators (possible risk factor but time ordering not established, cross sectional association demonstrated), risk market (fixed characteristic, e.g. sex, not amenable to change)
Putative risk factors for PD: diabetes, smoking, genetic susceptibility, poor OH
Diabetes & PD: Cohort study Pima Indians, high prevalence NIDDM, cases over 2x PD incidence of non-cases
Smoking & PD: evidence, review applied criteria for causation, concluded casual association, effects of smoking systemic
Paidi 1999: convenience sample current smokers (CS), former smokers (FS), non-smokers (NS), prevalence, extent & severity of LOA greatest among CS, lowest among NS, compared w NS, CS had 6x odds of 1+ sites w 6+mm LOA (3.5mm for FS)
Tobacco smoking behavioural risk factor for PD (effects via systemic route), incr cannabis use NZ (50%)
Confounding by cigarette smoking: statistically associated w both exposure & outcome of interest, control of confounders (randomisation, restriction, matching, stratification, modelling)
Methods – exposure variables: cig smoking (status prev year recorded @ ages, computed total pack-yrs exposure to age 32), cannabis smoking (# times in prev year)
Cannabis smoking associated w periodontal effects over those of cig smoking
Genetic susceptibility: >½ variation in pops, Kornman 1997 (high-risk genotype, test kit, clinical convenience sample), DMHDS (challenged validity of Kornman genotype, identified different genotype), genetic approach promising
Poor OH: biologically plausible, actual evidence poor, problems (amount plaque, composition, not much longitudinal evidence), plaque score @ 32 not associated w periodontitis prevalence or incidence in Dunedin study until longitudinally
Com level interventions: no universal additive like fluoride in water, cant change people’s genetics, main risk factors behavioural (smoking, diabetes – secondary to obesity, poor self care)
Smoking in NZ: prevalence decr from 20%, prevalence high in 15-34 age group, inequalities all ages, 1 in 2 Māori, 1 in 4 PIs, 1 in 5 Pakeha, social inequalities (beneficiaries, blue collar, white collar), healthy survivor effect
Implications: gr effects on public’s periodontal heath thru gen health promotion efforts decr smoking; healthy public policy (punitive taxes on tobacco), supportive environments (smokefree areas), com action (com groups), personal skills (OH advice), health services (GDP’s involvement in smoking cessation support)
Brady 2004: survey NZ dentists’ involvement in smoking cessation activities, barriers (lack of training, concerns about alienating pts, time req, resistance)
NZ smoking cessation guidelines: ABC format, A (ask status), B (brief advice stopping smoking), C (cessation support), multi-session, meds, assess nicotine dependence, refer
Conditions linked to PD (CVS disease, diabetes, pre-term birth), problems w research behind it (cross-sectional associations & wishful thinking, not controlled for confounders e.g. smoking)
Areas for epi research into PD: genetic basis PD (gene environment interactions), natural history disease, nature of association w systemic health, aetiology & natural of social inequalities, analytical approach for longitudinal perio data, pop level interventions