Periodontal Diseases- Etiology / Risk Factors

lecture given 11/6/2025

what factors affect a patient’s susceptibility to periodontal diseases?

nature and virulence of microbial challenge

individual’s oral ecology

robustness of host defense

genetic factors

local risk factors

systemic risk factors

risk factor

an aspect of personal behavior or lifestyle, an environmental exposure, or an inborn/inherited characteristic that changes the susceptibility to periodontal disease

can also be a local factor which increases the infection site

what kind of risk factors do cross sectional studies determine?

putative risk factors

what kind of risk factors do longitudinal studies determine?

true risk factors

evidence for causality- animal and in vitro studies of mechanism of action

what kind of risk factors do randomized clinical trials determine?

removal/modification of risk factors and measurement of disease outcome

cross sectional or case control studies

confounding factors are eliminated or adjusted for the analysis

longitudinal epidemiological studies (establish temporality and evidence for effects in casual pathway)

dose-response effects

mechanism studies

study results are consistent among various independent studies

intervention studies

effects are clinically meaninful, relationship is biologically plausible

t/f smoking is a risk factor for periodontal disease

true- there are a number of biologically plausible explanations for it as a causitive agent for periodontal disease

many prospective clinical studies have shown that smokers are more likely to develop periodontitis than smokers

risk indicator

associated with increased probability of disease, based upon cross-sectional studies carefully designed to eliminate those confounders that may result in a spurious associations

may be a probable or putative risk factor

if confirmed in a longitudinal study and determined to be in the causal pathway, they would be called risk factors

t/f herpesvirus is an example of a risk indicator of periodontal disease

true- the presence of herpesviruses in subgingival plaque is a risk indicator for periodontal disease

there is a biologically plausible explanation why herpesvirus may be causally related to periodontal disease but so far the evidence of association with disease is based on cross-sectional studies

risk marker

attribute or exposure associated with an increased probability of the disease

not usually factors or in the causal pathway but are somehow associated with the true risk factor

may be associated with the disease but are not in the causal pathway and if altered, may not affect the disease

t/f missing teeth are an example of a risk marker of periodontal disease

true- the number of missing teeth is a risk marker for disease but has little or no biological plausibility as a causative agent for periodontitis

are all risk factors modifiable?

no- some are but some (like genetics) are not

what is a modification to the risk factor of smoking?

smoking cessation

what is a modification to the risk factor of diabetes?

improve glycemic control

what is a modification to the risk factor of low dietary calcium?

calcium supplementation

what is a modification to the risk factor of osteoporosis/osteopenia?

bone-sparing agents, calcium, vitamin D supplementation

what is a modification to the risk factor of obesity?

diet and exercise

what is a modification to the risk factor of stress?

stress reduction measures

clear dose response

the more exposure to the risk factor, the greater the susceptibility to the disease

list local risk factors of periodontitis

tooth anatomical factors, dental restorations, orthodontic appliances, removable partial dentures, root fractures, cervical root resorption and cemental tears, caries, residual deep pocket depth, intrabody pockets (especially in furcations), root canal infections, calculus, local trauma, frenal attachments, mouth breathing and lack of lip seal

what do all local risk factors of periodontitis have in common?

plaque retentive

which diagnosis are local risk factors of periodontitis associated with?

VII A localized tooth related factors that modify or predispose to plaque induced gingival diseases/periodontitis

1- tooth anatomic factors

2- dental restorations/appliances

3- root fractures

4- cervical root resorption and cemental tears

developmental grooves

a developmental anomaly of the maxillary incisor teeth which has been reported to be associated with severe localized periodontal disease

presence of a palato-gingival groove is associated with poorer periodontal health and more plaque accumulation

t/f all maxillary incisor teeth with a palato-gingival groove will show localized periodontal destruction

false- not all 

what is the concavity mean distance from the CEJ to furcation entrance on maxillary premolars?

~7mm

what is the width of the furcation entrance on maxillary premolars?

~0.7mm

what percentage of maxillary 1st molars have a concavity on the

mesiobuccal root

distobuccal root

palatal root

94%

31%

17%

what percentage of mandibular 1st molars have a concavity on the 

mesial root

distal root

100%

99%

grade 1 cervical enamel projection

showing a distinct change in the cemento-enamel junction with enamel projecting towards the bifurcation

grade 2 cervical enamel projection

projection approaching the furcation, but not actually making contact with it

grade 3 cervical enamel projection

projection extending into the furcation

which arch molars are CEPs more common in?

mandibular

where are CEPs most prevalent?

maxillary and mandibular second molars

what are the most common grades of CEPs?

1 and 3

enamel pearls

furcation areas of the maxillary and mandibular 3rd molar roots

formed essentially from the hertwigs epithelial root sheath

sessile fusion with the root dentin

located apically to the CEJ

maxillary 3rd molars are more commonly affected

round, single, solid formation on root

radiopaque structure on root

pure enamel and sometimes dentin/pulp horn

root proximity

roots of teeth are abnormally close, makes it difficult to floss and keep clean

open contacts

lead to food impaction which leads to increased probing depth and increased CAL

biologic width

epithelial attachment (0.97mm) + connective tissue attachment (1.07mm) + sulcus (0.69mm) = 3mm

what about restorations can be a local risk factor for periodontitis?

roughness of the restorative material, rough/uneven tooth-restoration interface, overhang restorative material, marginal discrepancies, exposed cement margins, subgingival margins, overcontoured crowns

what can be done to restorations to avoid becoming a local risk factor to periodontitis?

contact areas should allow for the normal gingival papilla, supragingival margins are to be preferred where possible, where aesthetics are of concern margins should be placed less than 0.5mm into the gingival cervice, sufficient tooth reduction is required to avoid overbuilt crowns, a good impression technique with use of a gingival retraction cord, excess cement should be removed, hygienic pontics

what can be done to removable partial dentures to avoid becoming a local risk factor to periodontitis?

well supported with appropriate use of rest seats, 3mm clearance of the gingival margins, denture design should be kept simple, adequately maintained long term

calculus

rough irregular areas harboring plaque, plaque always forms on top of calculus, acts as a reservoir for periodontal pathogens and endotoxins, relatively sheltered from host defense, much of periodontal therapy is directed at calculus detection and removal

supragingival calculus

adjacent to openings of salivary ducts- lingual of mandibular incisors, buccal maxillary second molar

creamy white to yellow, may pick up extrinsic stains

mineral content is a mean of 37% of volume, derived from the saliva

mostly octacalcium phosphate and hydroxyapatite, some whitlockite, very little brushite

subgingival calculus

no predilection for particular parts of the mouth, interproximal and lingual sites more affected than buccal sites

brownish-black in color

mineral content is a mean of 58% by volume, derived from the GCF

whitlockite is the major constituent (it develops under anaerobic, alkaline conditions in the presence of Mn/Zn/carbonate), hydroxyapatite is also present, some octacalcium phosphate, no brushite

how can frenal attachments be local risk factors for periodontitis?

local plaque retention factor reducing access for OH, frenal pull means gingival recession

how can mouth breathing / lack of lip seal be local risk factor for periodontitis?

red, edematous, smooth gingiva

mainly maxillary anteriors

surface dehydration

higher levels of dental plaque

t/f there is a clear causal relationship between poor oral health and gingivitis

true- duh

can favorably influence the ecology of the microbial flora in shallow to moderate pockets, but it does not affect host response

has little effect on subgingival microflora in deep pockets

list systemic risk factors for periodontitis

smoking, diabetes mellitus, race/ethnicity, genetics/gene polymorphisms, male gender, PMN function, socioeconomic status, acquired systemic infections (HIV), severe malnutrition

list systemic risk indicators for periodontitis

low dietary calcium, obesity, stress, osteoporosis and osteopenia, decreased IgG2 antibodies

how can smoking act as a systemic risk factor for periodontitis?

exaggeration of inflammatory responses to periodontal pathogens, immune response suppression, direct toxic effect to cells, thermal effects, increased stains and calculus, effects on the oral flora, adverse effects of smoking on bone tissues resulting in reduced bone mineral density, suppresses hemorrhagic responses as measured by BOP, masking effect on the signs of inflammation, inhibition of growth an attachment of fibroblasts in the periodontal ligament, enhances the production of TNFa and causes the release of cytokines

smoking has been confirmed as a true risk factor for periodontitis in…

longitudinal studies with odds ratios for periodontitis in the range of 2.0-7.0

heavy smokers have odds ratios that are over ____ than that of light smokers for loss of attachment and bone loss

2x

smokers are also at increased risk for _______ following periodontal therapy

tooth loss

t/f 50% of patients with refractory chronic periodontitis are smokers

false- 90%

why is healing following mechanical treatment slower in smokers?

fibroblast inhibition, slower post treatment reduction of WBC and neutrophils

smoking appears to promote a favorable habitat for _______ bacterial species in ____ pockets

periodontopathogenic, shallow

type I diabetes (insulin dependent)

caused by an absolute insulin deficiency resulting from destruction from pancreatic beta cells, onset in childhood

type II diabetes (non-insulin dependent)

caused by impaired insulin function and a relative insulin deficiency, occurs in adulthood, associated with obesity

what measurements of A1c and FPG denote diabetes?

>= 6.5%

>= 126 mg/dl

what measurements of A1c and FPG denote prediabetes?

>=5.7% to <6.5%

>=100 mg/dl to <126 mg/dl

what measurements of A1c and FPG denote normal?

<5.7%

<100 mg/dl

what are the complications of diabetes mellitus?

retinopathy, nephropathy, neuropathy, vascular disease, altered wound healing, periodontal disease

t/f both type I and II diabetes are thought to lead to increased infections including periodontal disease

true

impaired protective immune response, impaired wound healing, induce a hyperinflammatory state associated with activated protein kinase C and advanced glycation of proteins, increased tissue destruction and greater levels of infection

poor diabetic control in the presence of calculus is associated wtih an increased frequency of probing depths 4mm

t/f diabetes and periodontitis has been studied since the 1990s with Pima Indians

true

t/f twin studies do not show any contributions of genetic factors

false- show significant contribution

there are over ___ associations between SNPs in candidate genes and periodontal disease

40

however, these are often not reproducible and differ among racial and ethnic groups

which genetic polymorphisms are the basis of tests which are marketed to assess periodontal risk?

interleukin 1B (IL-1B) gene

further SNPs on other interleukins have been investigated (IL-1A, IL-6)

which alleles are associated with an increased risk for developing severe periodontitis in non-smoking caucasian patients?

allele 2 of the IL-1A gene at nucleotide position -889 and the allele 2 of IL-1B gene at nucleotide position +3953

what are the outcomes of having allele 2 of the IL-1A gene at nucleotide position -889 and the allele 2 of IL-1B gene at nucleotide position +3953?

tooth loss, clinical and radiographic measures, severity of periodontitis

are males or females less susceptible to periodontal disease, and why?

females (at least pre-menopausal females)

because of the protective effects of estrogen on bone

what are examples of gender related temporary syndromes that may affect periodontal disease?

pregnancy associated gingivitis, puberty associated gingivitis

how is socioeconomic status a systemic risk factor for periodontal disease?

low educational levels and low income levels, increased stress, reduced access to dental care, lack of regular dental visits, lack of adequate oral hygiene which may result from cultural differences or lack of adequate knowledge about healthy behaviors

how are PMN abnormalities a systemic risk factor for periodontal disease?

congenital or acquired neutropenia, severe periodontal disease in childhood, early onset periodontitis in first molars/incisors (localized aggressive/juvenile periodontitis)

how is HIV infection a systemic risk factor for periodontal disease?

immune deficiencies, more susceptible to periodontal disease, linear gingival erythema

how is obesity a systemic risk indicator for periodontal disease?

adverse effects appear to be associated with the production of adipokines and cytokines by adipose tissue and by macrophages in adipose tissue

these pro-inflammatory molecules lead to a hyperinflamed state which probably increases tissue destruction triggered by periodontal and other infections

inflammatory mediated produced by adipose tissue (TNFa) are thought to also bring about insulin resistance which leads to diabetes and leads to increased risk for periodontal disease

how is low dietary calcium a systemic risk indicator for periodontal disease?

associated with increased periodontal disease in both men and women

the mechanism may involve reduced bone mineral density which renders the alveolar bone supporting the teeth more susceptible to periodontal infection

how is osteopenia/osteoporosis a systemic risk indicator for periodontal disease?

reduced estrogen levels lead to bone resorption outpacing bone deposition which sets the stage for more advanced periodontal bone loss associated with periodontal infections

calcium supplementation and bone sparing agents have shown modest effects in reducing tooth loss in older adults, suggesting that the modification of osteopenia may have a beneficial effect on alveolar bone

how is stress a systemic risk indicator for periodontal disease?

chronic stress and increased allostatic load appear to have many deleterious effects on the host including suppression of the immune response with increased susceptibility to infections

how is age a systemic risk factor for periodontal disease?

prevalence and severity of CAL has been associated with age in cross-sectional surveys

the current view is greater periodontal destruction in the elderly as reflecting lifetime disease accumulation rather than an age-specific condition

t/f it is common for elderly people with reasonable intact dentition to exhibit sudden bursts of periodontitis

false

t/f progression of periodontitis is considered to be a cyclical process- there appears to be extended periods of quiescence with short bursts of disease activity

true

the attachment loss that occurs during these bursts of disesase activity varies from a minor loss to relatively extensive destruction of the periodontium

in a study done from 2009-2010, over ____ of a sample (64.7 million adults) had periodontitis

___% mild

___% moderate

___% severe

47%

8.7%

30%

8.5%