JIDAM/Chennai/Volume:7/Issue:4/Pages 14

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JIDAM
“An Official Journal of IDA - Madras
Branch”©2020.
Available online

REVIEW ARTICLE

RISK FACTORS FOR PERIODONTAL

DISEASE- A REVIEW

Dr. Arunagiri, Dr. Anil Melath, Dr. Mohammed Feroz, Dr. Subair

Department of Periodontology,

Mahe Institute of Dental Sciences and Hospital, Chalakkara, Palloor, Mahe, Pondicherry,

India

Address for Correspondence:

Dr. Arunagiri,
Postgraduate Student, Department
of Periodontology,
Mahe Institute of Dental Sciences and
Hospital,
Chalakkara, Palloor, Mahe - 673310
Email id: giriarun133@gmail.com

Received

: 06.09.2020

Accepted

: 15.09.2020

Published

: 27.09.2020

ABSTRACT

A probability or threat of damage, injury, liability, loss, or any

other negative occurrence that is caused by external or internal

vulnerabilities, and that may be avoided through pre- emptive

action is called as risk. This article explains about the evidence

on the potential role of modifiable and non-modifiable risk

factors associated with periodontal disease. It is important to

understand the etiological factors and the pathogenesis of

periodontal disease to recognize and appreciate the associated

risk factors. As periodontal disease is multifactorial, effective

disease management requires a clear understanding of all the

associated risk factors. The local factors include pre-existing

disease as evidenced by deep probing depths and plaque

retention areas associated with defective restorations. Systemic

risk factors recently have been identified by large epidemiologic

studies using multifactorial statistical analyses to correct for

confounding or associated co-risk factors. The study of risk in

periodontal disease is a rapidly emerging field and much is yet

to be learned.

KEYWORDS:

Periodontal disease, risk factors, host response,

risk assessment

To access & cite this article

Website: jidam.idamadras.com

DOI:1.37841/jidam_2020_V7_I4_03

Arun et al : Periodontal disease risk factors

146

Periodontal disease is a group of persistent infections
induced via pathogenic microorganisms that
colonize the periodontium. The onset and
progression of periodontal infections are influenced
through local and systemic conditions. Local
elements consist of dental plaque and retention
areas of the plaque, such as dental calculus and
faulty restorations. Systemic risk elements consist
of poorly managed diabetes mellitus and smoking.
Systemic prerequisites

related with

immunodeficiency, such as neutropenia, AIDS
/ HIV infections, are additionally essential hazard
factors. Recent research has published countless
probably necessary periodontal risk indicators

These consist of stress and coping behaviors and
osteopenia related with estrogen deficiency. There
are additionally demographic elements related with
periodontal disease, which include gender, and
hereditary factors.

TERMINOLOGIES:

Risk (Kleinbaum 1982): It is the probability that an
individual develops a certain disease or exposure or
changes the state of health in a given period.

Risk factor: - It is an environmental exposure,
a behavioral aspect or an intrinsic characteristic
associated with a disease. - To be identified as a risk
factor, exposure must occur before the onset of the
disease

Risk indicators: - They are probable and putative risk
factors that have been identified in cross-sectional
studies but not confirmed through longitudinal
studies. - They are not believed to be part of the
causal chain.

Markers or risk predictors: These are characteristics
that have the ability to predict high risk individuals,
but are not part of the causal chain. They can predict
the future course of the disease. Risk determinants:
These forms, sometimes replaced by the term risk
factor, should be reserved for those risk factors that
cannot be changed, are probably not in the causal
chain and are not the objectives of the intervention.
Risk assessment: - It is the process of determining
the quantitative and qualitative probability of adverse
events that can result from exposure to specific health
risks or the absence of beneficial influences.

RISK

FACTORS

PERIODONTAL

DISEASE

MODIFIABLE RISK FACTORS:

MICROORGANISMS AND PERIODONTAL
DISEASE;

Of all a variety of microorganisms that

colonize the mouth, there are three, Porphyromonas
gingivalis,

Tannerella forsythia (formerly

Bacteroides forsythus) and Actinobacillus
actinomycetemcomitans which have been implicated
as causative agents in periodontitis

SMOKING:

Cross-sectional and longitudinal records

provide strong aid that the risk of growing
periodontal disease measured by means of loss of
clinical attachment and loss of alveolar bone will
increase with increasing smoke

. Studies have

proven that smoking no longer minimizes the
amount of plaque existing and, in fact, smokers may
additionally experience much less gingival bleeding
than nonsmokers with decrease in plaque indices. It
has been suggested that this reflects an alteration
in the size of the blood vessels which makes the
gingival tissues perfect. It has also been suggested
that the reduction in bleeding reflects an underlying
disruption of the immune response and that this
could explain the greater loss of clinical attachment
and alveolar bone

DIABETES MELLITUS:

One of the important oral signs of diabetes

is gingivitis and periodontitis. Both type 1 and type
2 diabetes mellitus are related with excessive
degrees of systemic markers of inflammation. The
excessive inflammatory status in diabetes contributes
to microvascular and macrovascular issues and it is
clear that hyperglycemia can trigger the activation of
pathways that enlarge inflammation, oxidative stress
and apoptosis

. Elevated serum IL-6 and TNF-

ranges have been validated in diabetes and obesity,
and serum IL-6 and C-reactive protein (CRP) ranges
have been proven  to  predict  the  future  onset  of
diabetes  mellitus type  2.  High  ranges  of  CRP  are
additionally related with insulin resistance, type two
diabetes mellitus and  cardiovascular  disease.  TNF-

α and IL-6 are the

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147

primary inducers of acute phase proteins, including
CRP and each have been shown to alter the signaling
of intracellular insulin, which may additionally
contribute to insulin resistance. Serum IL-6 and
CRP levels are additionally increased in patients
with periodontitis, with IL-6 levels associated to the
spread of the disease. Systemic irritation associated
with periodontal  disease can consequently enhance
the diabetic status. Adipokines may additionally also
contribute to susceptibility to both periodontitis and
diabetes,  and  the  proinflammatory  properties  of
leptin may  additionally  be  especially  essential  in
regulating periodontal  inflammation  in  overweight
and / or type two diabetes mellitus

CARDIOVASCULAR DISEASE:

The biological plausibility of the association

between periodontal diseases and cardiovascular
diseases is well studied and it includes some of the
following possible mechanisms: high concentrations
of cholesterol and the action of oral bacteria in the
process of atherosclerosis or the participation of
acute-phase proteins that may increase in chronic
periodontitis

.Varied biological mechanisms have

been proposed to provide an explanation for the
relationship between periodontal and cardiovascular
diseases. Therefore, periodontitis can probably elicit
a systemic inflammatory response and it deserves
more attention. Periodontal disease is capable of
predisposing to vascular diseases due to the
prosperous supply of subgingival microbial species
and the host’s response. Furthermore, we must be
aware that these diseases share many risk factors
and there are evident similarities to the basic
pathogenic mechanisms

. Periodontitis is associated

with  increase in the level of C-reactive protein and
fibrinogen, irrespective of coronary diseases.
Furthermore, there is evidence that suggests that
the increase in  the  levels  of systemic markers
of inflammation, such as the C-reactive protein
(CRP) and interleukin-6 (IL-  6), is associated with
cardiovascular diseases.

Bacteremia from periodontitis and dental

disease is known to be the primary cause of infective
endocarditis. In particular, patients who have
undergone heart valve surgery have a significant
risk of life-threatening infective endocarditis.
Epidemiological and microbiological studies have
lent credence to the concept that periodontal disease

may be a separate risk factor for cardiovascular
disease, cerebrovascular disease, and preterm
delivery of low birth weight infants.

Wu et al

have proven that periodontal disease is

any other putative and independent risk element for
cerebrovascular disease, specifically for ischemic
stroke. In 1989, Kimmo Mattila and his co-workers in
Finland conducted two separate case control studies
totaling 100 patients with acute myocardial infarction
and they compared these patients with 102 control
subjects selected from the community. A dental
examination was performed on all the patients and
a dental index was computed. In this original report,
subjects with evidence of oral infection were 30%
more likely to present with myocardial infarction
as against subjects without oral infections. Janket et
al performed a meta-analysis of nine cohort studies
of PD as a risk factor for future cardiovascular and
cerebrovascular events RR 1.19; (95% CI [1.08–
1.32]) and found an overall 19% increased risk of
such events in individuals with periodontitis. The
increase in risk was greater (44%) in people under
age 65. However, Garcia RI et al 2010 and Trevisan M,
Dorn J et al 2010 have not discovered a relationship
between periodontitis and ischemic coronary heart
disease.

DRUG INDUCED DISORDERS:

Irrespective of the causative medication,

the clinical appearance of drug-induced gingival
overgrowth remains the same, with the onset usually

occurring 1−3 months following commencement of
the medication. The dosage of medication, combined
with the amount of dental plaque and periodontal
inflammation, is linked to the prevalence and severity
of the overgrowth seen. The anterior gingiva is one
of the most commonly affected sites. The overgrowth
begins normally in the interdental papilla region and
spreads to cover the buccal and palatal surfaces of the
teeth. Although largely a cosmetic concern, due to
the overgrowth causing a reduction in clinical crown
height and, in some cases, completely obscuring the
teeth; the enlargement can also cause speech and
masticatory difficulties, especially in young children.
Fibrosis can occur in chronic overgrowth cases,
leading to tooth migration and possible secondary
malocclusion in the presence of altered masticatory
habits. Enlargement of the interdental papillae can
also lead to displacement of teeth and thus resulting
in diastema. Although the gingival enlargement is

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not directly harmful, inflammatory changes become
apparent due to the difficulties in plaque control,
leading to oedema, erythema and bleeding. This
appearance is commonly encountered in the presence
of preexisting periodontal disease.

Some drugs drastically minimize salivary

flow.  These consist of antihypertensives, narcotic
pain relievers, some tranquilizers and sedatives,
antihistamines and antimetabolites. Other drugs,
specifically those in liquid or chewable form that
contain added sugar,  alter the pH and composition
of the plaque, and facilitating  adherence  to the
surfaces of the teeth

. Drugs can be a contributing

factor to periodontal disease. Drugs such as
anticonvulsants, calcium channel blocking agents
and cyclosporine can result in overgrowth of the
gums

. In 1996, Seymour et al postulated the

concept of genetic predisposition for DIGO
etiopathology. This is proven by way of the truth
that some humans develop gingival hyperplasia and
others do not while taking the same drug. The ordinary
inflammatory response of the gingival fibroblasts and
the consequent proliferation of the connective tissue
matrix underlines the heterogenetic character  of
the gingival fibroblasts in response to the inducer
drugs. The frequent mechanism of action at the cell
stage of these three extraordinary classes of tablets
appears to be the inhibition of the entry of cations,
in precise sodium and calcium ions. Clinicians
accept  the truth that gingival overgrowth  is
multifactorial,  bacterial  plaque  appears to  be  a
contributing  factor  and  the  severity  of  gingival
overgrowth is believed to be at once proportional
to the degree of plaque accumulation and plaque-
induced inflammation. The decreased transport of
energetic cation-dependent folic acid (FA) inside the
gingival fibroblasts reasons a decreased absorption of
FA by using cells, inflicting adjustments in the matrix
metalloproteinase metabolism and lack of ability to
set off collagenase. This causes  the accumulation
of connective tissue and collagen due to the lack of
collagenase triggered through DIGO.

Patients with gingival overgrowth may be

at an increased risk of periodontal disease, as well
as tooth decay. Gingival overgrowth creates pseudo
pocketing coronal to the cementoenamel junction,
which may hinder effective plaque control. In
periodontally susceptible patients, this may progress
to loss of periodontal attachment. Another recent

study reported that patients who take nonsteroidal
antiinflammatory drugs regularly are prone to the
development of aphthous ulcers or lichenoid type
lesions. Not only are these patients at increased risk
for occurrence of these lesions, but they are more
prone to recurrence of these lesions.

STRESS:

The term stress serves as a convenient

description for complicated and incomplete
psychological

andphysiological

phenomena.

Anxiety, as well as different emotional or
psychosocial

tensions,

produce properly

characterized neuroendocrine and biochemical
modifications in experimental animals. Patients with
insufficient stress behavioral techniques (defensive
coping) are at elevated chance of extreme
periodontal disease

OBESITY:

Obesity has been stated to be a vital

chance element for periodontal disease. Various
explanations have been provided for the association
between weight problems and periodontal disease in
younger adults. Young humans can also have unique
eating regimen plans than older study participants.
Research on dietary developments in teens aged 11
to 18 exhibits a huge reduction in uncooked fruits
and greens except potatoes, which are sources of
vitamin  C.  In  addition,  teens  have  diminished  their
calcium consumption and improved consumption
tender drinks instead than citrus juices. This is
essential for oral fitness due to the fact that  low
dietary calcium  and  vitamin  C  consumption  has
been  related with periodontal disease. People who
eat much less than the encouraged each day
allowance (RDA) for calcium  and  vitamin  C  have
barely greater charges of periodontal disease

NON-MODIFIABLE RISK FACTORS

OSTEOPOROSIS:

Many of the studies conducted to date suggest

there is a relationship between skeletal osteoporosis
and bone loss

to the extent that postmenopausal

osteoporosis may result in dental osteopenia
involving the jaws, and particularly the mandible.
Osteoporosis was once extensively related with

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Arun et al : Periodontal disease risk factors

extreme alveolar crestal bone loss and the occurrence
of periodontitis cases in postmenopausal women.
A review of the relationship between osteopenia,
oral bone loss, and periodontal disease concluded
that osteopenia does play a role in the expression
of periodontal disease. The evaluation indicated a
direct association between skeletal and mandibular
osteopenia and loss of alveolar crestal height and
enamel loss in postmenopausal females. Taguchi et
al have stressed that it is important to distinguish
among osteopenia, which has been defined in general
terms as a decrease in normal mineralized bone,
postmenopausal osteoporosis, which is a disease
caused by the cessation of estrogen production and
characterized by spinal fractures that occur between
the ages of 50 and 70 years, and osteoporosis, which
affects an older population and results in proximal
femur fractures. Periodontitis and osteopenia
may have common etiological agents that may
either directly influence or modulate both disease
processes

HEMATOLOGICAL DISORDERS:

Hemorrhagic gingival overgrowth with or

without necrosis is a frequent early manifestation
of acute leukemia. Chronic leukemia patients may
additionally experience similar but much less
extreme periodontal changes. Chemotherapy or
remedy related with bone marrow transplantation
can additionally adversely have an effect on gingival
health

HOST RESPONSE:

Chronic periodontitis includes complex

interactions between microbial elements and sensitive
host. Bacterial elements such as lipopolysaccharides
and cytokines activate macrophages to produce
cytokines such as interleukin (IL) -1 and tumor
necrosis issue (TNF). These cytokines activate the
fibroblasts that stay in the periodontal tissues to the
matrix metalloproteinases (MMP), a plasminogen
activator, which can activate the plasmin. Plasmin,
in turn, can activate some other sorts of latent MMPs,
while tissue metalloproteinase (TIMP) inhibitors can
inactivate active MMPs. Prolonged and excessive
bacterial promotions of MMPs amongst sensitive
men and women result in an enchancement in the
degradation of collagen, which is a necessary factor
of the periodontal matrix. MMP-8 and -9 are released

from polymorphonuclear leukocytes (PMN) and
are accountable for a tremendous section of the
destruction precipitated through the host response.
MMP-13 additionally enables bone resorption by
using degrading the collagen matrix of the bone after
the bone is demineralized by means of osteoclasts

PREGNANCY:

Offenbacher et al discovered extensively

higher periodontal attachment loss amongst mothers
of PLBW toddlers than mothers of term infants.
Likewise, quite a few different researches have
advised a poor effect of periodontal disease on the
direction of pregnancy. It has been recommended
that periodontal disease might also make bigger the
risk of having low birth weight premature infants
(PLBW). This end result is believed to be the effect
of biological mediators of inflammatory methods
such as prostaglandins E

and TNF. The frequent

bacterial product lipopolysaccharide may also have
a triggering function at some stage of pregnancy

RISK ASSESSMENT:

When risk assessment is performed without

the use of a risk assessment model, there is a
large degree of variation between general dentists
and Periodontists and between the Periodontists
themselves, so it is important to develop risk
assessment models.

DEVELOPMENT OF THE MODEL:

Lang and Tonetti, 2003

model is a continuous

multilevel risk assessment model that incorporates
subjective assessments of dental and site risk and
generates a functional diagram and, according to the
area of the polygon, classifies the patient into low,
medium and high-risk categories (Fig. 1).

Fig 1: Lang and Tonetti’s periodontal risk

assessment (PRA)

model (Lang and

Tonetti, 2003; Lang et al, 2003).

149

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However, the original model has the following
limitations:
• Mainly assesses the cumulative status of a patient
with periodontitis
• There is no adequate identification of risk factors
and risk determinants
• In the functional diagram, the presence of a systemic
disease is assessed as a high-risk factor without
emphasis on the current state of a disease
• Smoking is assessed in the risk assessment model,
but another potential risk factor, diabetes, is not
assessed separately and is included in the category of
systemic diseases
• Does not take into account various dental factors,
which can modify or initiate the progression of
periodontal disease.
Four entities from the original risk assessment
model were maintained in the new model:
bleeding on probing (BOP), depth of survey, tooth
loss and smoking (the latter was described under
“environmental factors” in the original model). The
entities that were added to the new model included
various aspects of risk assessment, in particular risk
factors (diabetes and dental deposits or factors that
can hold deposits) and other factors that determine
risk such as socioeconomic factors and stress (Page
and Beck, 1997)

The risk assessment model included eight
parameters:
1. Percentage of sites with BOP
2.

Number of sites with probing depth (PD) ≥ 5 mm

3. Number of missing teeth
4. Loss / attachment ratio (AL) / age
5. Diabetic state
6. Smoking
7. Dental state: interaction of systemic factors
8. Other background features

BOP, PD, tooth loss and AL / age ratio measure the
cumulative periodontal status, which is the current
state of the individual due to periodontal disease.
Diabetic status and smoking are risk factors and stress
and socioeconomic factors are the determinants of
risk, which have been assessed in this new model.
However, all of these parameters were assessed on
a five-point risk scale to balance the sensitivity of
the risk assessment with the time and experience
required to collect the required information (Page et
al, 2003)

CONCLUSION:

It is imperative that the dentist look beyond the

oral cavity in search of factors to recommend changes
in order to help his patients achieve their common goal
of prevention or management of periodontal disease,
and therefore possibly also improve overall health
and it is also important to understand the etiological
factors and the pathogenesis of periodontal disease to
recognize and appreciate the associated risk factors.
Since periodontal disease is multifactorial, effective
disease management requires a clear understanding
of all associated risk factors.

FINANCIAL SUPPORT AND
SPONSORSHIP:

Nil

CONFLICTS OF INTEREST:

There are no conflicts of interest.

Arun et al : Periodontal disease risk factors

151

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