lec2

discipline studying DISTRIBUTION and DETERMINANTS of health problems

"how many" and "which" persons affected, to "degree of severity"

factors that may play a role for disease pathogenesis

effects of specific measures for controlling/preventing diseases

prevalence, severity, extent

number of individuals who have caries at a specified point in time, divided by total individuals in study population at same time

severity of lesions counted

number of teeth or surfaces w caries

D1: incipient enamel lesions, no cavitation
D2: enamel caries with loss of structural continuity
D3: dentin caries
D4: dentin caries w pulp involve

sum of number decayed, missing due to caries, and filled teeth

questionable to give equal weight to untreated caries, restos, missing teeth

DMFT does not estimate tx needs

teeth can be missing for various reasons

missing tooth counted as 4/5 surfaces -> overestimation

filled surface determined by operator design

implies that caries level at one age predicts caries lvl at later age

% of caries free individuals

% caries free individual increases
caries distribution contracts

directly related (if one is positive linear, other is positive linear too)

discipline studying DISTRIBUTION and DETERMINANTS of health problems

D4 and D3

the only caries we can detect clinically are D3 and D4

we do not have the means to detect the "under the surface" carious lesions like subclinical, D1, D2 and so on

so just because we do not see caries, does not mean there are no caries

lesions on natural, intact tooth surfaces

lesion developing at a tooth surface adjacent to a filling

demineralized tissue that was left behind before filling placed

loss of continuity of enamel and/or dentin

enamel surface intact

lesion is progressing, can develop further later if not interfered

lesion formed years before, stopped further progression

multiple carious lesions in the same patient

involves surfaces that usually dont have caries

called bottle or nursing caries in children

called bakers' caries, radiation caries, and drug-induced caries in adults

early childhood caries, teeth exposed to carbs and located where oral clearance is low (max incs)

beneath contact facets proximally extending onto B/L as DULL, CHALKY WHITE enamel along gingival margin

particular shape of stagnation area

yes; but NOT ALL WSL ARE INCIPIENT (some may be arrested for years)

increased porosity > stain uptake

V-type: wide at top, gradually narrow at bottom (34%)
U-type: 14%
I-type: extremely narrow slit
IK-type: extremely narrow slit with large space at bottom (26%)

V type

small, deep well originating on L/O/B of molars

chalky white opaque lesions
evident only under dry conditions
extend along groove/pit
WILL get plaque when probing

clinically seen as DARK, STAINED (dark brown to black) p/f
hard on probe
little-no plaque accml

enamel look bluish long fissure (undermined enamel)
opening cavity > significant destruction of tooth

active lesion w large cavity deep into dentin
or
arrested lesion w hard, painless and stained dentin

active, non-cavitated smooth surface caries

no; one tooth can have all 4 types

CHALKY WHITE APPEARANCE(why drying is impt)

caries will be DULL, CHALKY, and non-translucent

1st statement is false; not all cavitated lesions are active (they may be arrested)

if pt improves oral hygiene, inflamed gums will recede back to normal levels, such that lesion is no longer at the gingival margin (due to margin lowering back)

development of granulation tissue in response to persistent, low grade mechanical irritation and bacterial invation of pulp

reactive hyperplasia of gingiva to local irritants