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risk
the probability of an individual to develop a specific disease in a given period which may vary from one individual to another
either predisposes to develop periodontal dx or influence the progression of an existing dx
risk elements are:
risk factors
risk determinants
risk indicators
risk predictors / markers
risk assessment
involves identifying elements that either predispose a patient to developing periodontal disease or influence progression of a disease that may already exist
risk factors
are environmental, behavioral or biologic factors
when present, increases the likelihood that an individual will develop the disease
identified through longitudinal studies of patients with the disease of interest
exposure to this factor may occur at a single point in time; over multiple, separate points in time; or continuously.
the exposure must occur before disease onset
examples of risk factors
tobacco smoking
diabetes mellitus
pathogenic bacteria & microbial tooth deposits
severe periodontal disease
has been found to be a significant risk factor for poor glycemic control
anatomic factors that at risk to periodontitis as they harbor bacterial plaque and present
furcations
root concavities
developmental grooves
cervical enamel projections
enamel pearls
bifurcation ridges
3 specific bacteria etiologic agents of periodontitis
Actinobacillus actinomycetemcomitans
Actinobacillus actinomycetemcomitans - old term
Porphyromonas gingivalis
Tannerella forsythia
Aacteroides forsythus - old term
are common sites with root proximity complications.
mx 1st & 2nd molars
biologic width
represents the anatomic dimensions of the epithelial attachment and the connective tissue attachment.
A restoration that does violate this would initiate a chronic inflammatory condition that results in bone and attachment loss to reestablish the dimensions
risk determinants
aka: background characteristic
these are risk factors that cannot be modified
examples of risk determinants
age
genetic factors
socioeconomic status
gender — males are more prone to periodontitis
stress — incidence of ANUG increases during stressful periods
risk indicators
aka: putative risk factors
are probable that have been identified in cross-sectional studies but not have been confirmed through longitudinal studies
factors associated with periodontal disease but not yet proven to be causative due to insufficient evidence
examples of risk indicators
osteoporosis
infrequent dental visits
HIV / acquired immune deficiency syndrome
risk markers / predictors
these are associated with increased risk for disease but do not cause the disease
examples of risk markers / predictors
previous history of periodontal disease
bleeding on probing — together with increased pocket depth may serve an excellent predictor for future attachment loss.
pregnancy
development of pyogenic granuloma
a reactive hyperplasia in response to local irritants, hormonal factors
gingiva on anterior teeth as most common site
scorbutic gingivitis
gingivitis due to vit C deficiency
a diabetic patient with a HbA1c of 9.5%
a patient would be expected to be at greatest risk for periodontal disease
smoking
a well-known risk factor for chronic periodontitis
The risk for periodontal disease after smoking cessation lowers continuously.
In the first few years after smoking cessation, the risk ranges between the risk for smokers and that for never-smokers.
Three years following smoking cessation, the risk for periodontal disease is three times higher in former smokers when compared to the risk of never smokers.
After eleven years, the risk for periodontal disease is similar between former smokers and never-smoker
grade I furcation involvement
incipient bone loss or early lesion
interradicular bone is intact
depression on furcal opening described as dimples
grade II furcation involvement
partial bone loss
moderate loss of interradicular bone
probe enters opening of furcation but not through & through
CUL-DE-SAC lesion
grade III furcation involvement
total bone loss
through & through furcation involvement that can only be seen radiographically
grade IV furcation involvement
total bone loss
through & through furcation involvement with gum recession that is clinically visible
plaque-induced gingival diseases
most common
result of interaction between plaque bacteria & inflammatory cells of host
modified by systemic factors, by medications, by malnutrition
non-plaque-induced gingival diseases
less common
in response to infections
in response to allergy
in response to trauma
gingival lesions of genetic origin
chronic periodontitis
older px (55 y.o)
any arch is affected
no familial aggregation
slow to moderate attachment loss
horizontal (suprabony) pattern of bone loss
consistent destruction in relation to microbial deposits
often commensurate with observed periodontal destruction
aggressive periodontitis
young px (<35 y.o)
rapid attachment loss
yes to familial aggregation
first molar & incisors are affected
often minimal presence of plaque
vertical / angluar (infrabony) pattern of bone loss
inconsistent destruction in relation to microbial deposits
causative agent of localized aggressive periodontitis (LAP)
aggregatibacter actinomycetemcomitans (Aa)
causative agent of generalized aggressive periodontitis (GAP)
porphyromonas gingivalis
causative agent of necrotizing ulcerative gingivitis (NUG)
spirochetes
causative agent of necrotizing ulcerative periodontitis (NUP)
fusiform bacteria
bacterias found in chronic periodontitis
P. gingivalis and T. forsythia
other etiologic factors in periodontitis
Campylobacter rectus
Eubacterium nodatum
Fusobacterium nucleatum
Prevotella intermedia/ nigrescens
Peptostreptococcus micros
Streptococcus intermedius
Treponema denticola
calculus
reservoir for bacterial plaque
has been suggested as a risk factor for periodontitis
Although the presence of some calculus in healthy individuals receiving routine dental care does not result in significant loss of attachment, the presence of calculus in other groups of patients, such as those not receiving regular care and patients with poorly controlled diabetes, can have a negative impact on periodontal health
associated with severe chronic periodontitis in nonsmoking subjectss
interleukin-1α (IL-1α)
interleukin-1β (IL-1β)
—Overall, it appears that changes in the IL-1 genes may be only one of several genetic changes involved in the risk for chronic periodontitis. Therefore, although the alteration in the IL-1 genes may be a valid marker for periodontitis in defined populations, its usefulness as a genetic marker in the general population may be limited
IgG2
the antibody response to A. actinomycetemcomi- tans in patients with aggressive periodontitis
age
as a risk determinants
Although periodontal disease is more common and severe in older individuals, this is mainly due to cumulative exposure to risk factors over time, not aging itself.
Studies show that people who maintain good preventive care throughout life have minimal attachment loss, indicating that periodontal disease is not an inevitable consequence of aging.
However, age-related changes (e.g., medications, reduced immunity, poor nutrition) may interact with other risk factors and increase susceptibility, but this is not yet fully established.