Volume 7, Issue 3, March – 2022 International Journal of Innovative Science and Research Technology

ISSN No:-2456-2165

Personalized Periodontics
Dr. Christy George, Dr. Abhijith Shetty Dr. Nandini Manjunath
Post Graduate Head of Department
Department of Periodontology and Implantology Department of Periodontology and Implantology
A J Institute of dental sciences, Mangalore, India-575004 A J Institute of dental sciences, Mangalore, India-575004

Abstract:- The introduction of personalized periodontics concept in which networked individuals will take a leading
is an exciting step toward a medical paradigm of disease role in their own health care.
management, namely, the recognition of the individual as
the fundamental component in the management of Personalized periodontics is one part of the 4 P approach
extremely complicated diseases. Tobacco, uncontrolled to treatment. Individual differences in genetic variables,
diabetes, obesity, cardiovascular disease, and stress must circumstances, lifestyles, and behaviour are all taken into
all be considered in a recreational approach for account in personalised periodontics. As a result, personalised
comprehensive periodontal disease therapy. periodontics is defined as the division of patients into distinct
groups and the tailoring of clinical decisions, procedures,
The many components of individualised and/or products to each patient.
periodontics are discussed in this review.
II. IDENTIFYING INDIVIDUAL RISK FOR
I. INTRODUCTION PERIODONTITIS

Periodontal disorders are regarded to be complex To identify individual risk for periodontitis, a set of risk
diseases with varying treatment outcomes. While bacteria are factors must be individually validated. Since there are
the cause of periodontal disease, the individual's multiple risk factors for a chronic disease like severe chronic
inflammatory response as well as other modifying and periodontitis, a mechanism to stratify patients utilizing
predisposing factors ultimately determine the clinical combinations of various risk factors must be used.[4]
presentation and outcome. Disease progression is influenced  Step 1: Identify probable periodontitis risk factors.
by environmental and genetic factors that are unique to each To find specific characteristics that are linked to patient
person. When diagnosing, treating, and managing differences in periodontal clinical indicators, progression or
periodontal diseases, the individual's specific inflammatory severity, treatment response, or systemic consequences of
response and associated regulating factors must be taken into periodontitis.
account.
 Step 2: Putative risk factors must be clinically validated.
As a result, there is now a clear need to identify
individuals with advanced and complex illness and find  Step 3: Clinical utility necessitates the use of risk
preventive or treatment measures that may be used to control variables to categorise people into groups in order to
the oral (and likely systemic) implications of periodontal guide illness prevention and treatment.
diseases on an individual basis.
Predefined parameters that stratify every patient into
Personalized medicine is a medical approach that well-defined categories that are mutually exclusive are the
emphasizes tailoring oral healthcare decisions, practices, first step in individualising periodontitis risk and prevention
and/or products to the specific needs of each patient. [1] and therapy.
Predictive, personalized, preventative, and participative
features are included in the 'P4 medicine' concept, which is III. RISK FACTORS AND INDIVIDUALIZED
an extension of personalized medicine. [2] The term 'P4 TREATMENT APPROACH
medicine' was coined by Leroy Hood [3] more than 5 years
ago to describe a continuing shift in medicine from a reactive Tobacco use, uncontrolled diabetes, obesity,
to a proactive discipline, with the ultimate goal of cardiovascular disease, and psychological stress are all
maximizing wellbeing for each individual rather than simply presented in the context of how different lifestyles must be
treating the disease. incorporated into a tailored periodontal disease management
strategy.[5]
 A Predictive strategy based on the use of high-tech
diagnostic techniques will allow us to identify at-risk The knowledge of risk factors aids in the detection and
patients and diagnose periodontitis early, when it is simpler treatment of periodontitis pathobiology, because risk varies
to treat successfully. widely from one person to the next. A patient-centered,
 It is a tailored Prevention based on a specific patient's individualised treatment plan is created and implemented.
genetic and microbiological status.
 Personalized treatment based on the patient's unique
medical situation.
 The patient's active engagement will be highlighted with
the introduction of Participatory periodontology, a

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Volume 7, Issue 3, March – 2022 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
A. SMOKING smokers than in smokers. In terms of vertical and
Tobacco use, in all forms, has a negative impact on both horizontal attachment gain, smokers had a poorer
periodontal disease and peri-implant conditions, and is healing outcome after surgery. The healing of a GTR-
strongly linked to altered microbiology, host/inflammatory treated infra-bony defect is hampered by smoking. [11]
responses, and genetic traits that are unique to each tobacco- In terms of pocket depth reduction and attachment
using patient. level gains, smokers respond less favourably to flap
debridement surgery.[12]
a) Microbial considerations
Smokers showed a higher prevalence of dental plaque
than non-smokers suggested that more severe
periodontal disease in smokers might be because of
greater accumulation of plaque.

In smokers, studies have shown significantly

higher periodontal pathogen recovery rates [6],earlier
establishment of periodontal pathogenic bacteria into
the biofilm, less reduction in periodontal pathogens
following scaling and root planing[7],diminished
healing response to systemic antibiotic regimens [8],
and a shorter rebound period to a pathogenic flora
following resolution of gingival inflammation.Shifts
in biofilm ecology toward a microbiota associated
with periodontal health, were reported following
successful smoking cessation.[9]

b) Host response considerations

Acute exposure to high concentrations of tobacco
constituents during smoking and chronic exposure to
compounds that persist in the tissues, saliva, and GCF
at low concentrations following tobacco use
significantly alter the interactions between the host
response and the oral microbiota. [10]The major  Management
driving force in periodontal breakdown, is an There are a number of approaches that can be used to give
imbalance between the protective and individual advice to smokers. This can vary from ‘very
destructive/inflammatory functions of the host brief advice', where attention is drawn to the smokers'
response. habit, 'brief advice' including 5 step programme and is a
more detailed advice such as that given by the specialist
The first host-response events occur in the smoking cessation services.
periodontal pocket between the plaque biofilm and
neutrophils that have migrated out of the tissue, aided Very brief advice
by complement and antibody. These neutrophils The goal of this advice is to call attention to smokers,
migrate to the plaque biofilm and engulf the target their habits, and to provide guidance on how to quit
bacteria. smoking in under three minutes. Rather than increasing
cessation rates, this advice's major effect would be to
The defensive capabilities of neutrophils, such stimulate attempts to quit.
as chemotaxis and phagocytosis, can be harmed by
products found in cigarette smoke. Smoke also causes Brief advice
neutrophils to generate tissue-destructive chemicals Brief advice for the patient to stop smoking may last
such as superoxide and hydrogen peroxide. for around l0 min.
The GCF of smokers with periodontitis has A 5-step program recommended by the Agency for
higher amounts of RANKL and lower levels of the Health Care Research and Quality, which uses the five A's
bone-protective OPG. Nicotine can slow healing by -
diminishing fibroblast adhesion and lowering  Ask - Identify patients tobacco use status
collagen synthesis, among other things.  Advise - On association between oral disease and
smoking and the benefits of quitting.
c) Effects of Smoking on Response to Periodontal  Assess –Determine patient’s interest and willingness
Therapy to participate in tobacco cessation programs
After non-surgical periodontal therapy, which  Assist – Use right strategies to help patient quit
includes scaling and root planing as well as systemic smoking
or locally administered adjuvant metronidazole, the  Arrange - Follow-up contacts with the patient
reduction in pocket depth is more successful in non-

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Volume 7, Issue 3, March – 2022 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
 Management
Periodontal health is harmed by poor glycemic control,
and periodontitis can affect a diabetic's glycemic state.

If a patient is suspected of having undiagnosed diabetes,

lab testing, including fasting blood glucose and random
glucose, are performed. If a patient has diabetes, it is vital to
determine the level of glycemic control before beginning
periodontal treatment. Oral hygiene recommendations,
mechanical debridement to eliminate local causes, and
frequent maintenance should be given to diabetic individuals
with periodontitis.

Fig. 2

The therapeutic goal for many patients is to achieve and

maintain an HbA1c below 8%. Patients with relatively well-
controlled diabetes (HbA1c < 8%) usually respond to therapy
Fig. 1
in a manner similar to nondiabetic individuals. Poorly
B. DIABETES MELLITUS controlled patients (HbA1c >10%) often have a poor response
Diabetes is one of the major risk factors for periodontitis. to treatment, with more postoperative complications and less
Individuals with diabetes are more likely to have favourable long-term results. Improvements in HBA1c values
periodontitis of increased severity when their diabetes is after periodontal therapy may provide an indication of the
uncontrolled or poorly controlled. Periodontitis is now potential response.
considered to be the 6th complication of diabetes.
Before undergoing surgical treatment, a HbA1c of less
Diabetes contributes to increased inflammation in the than 10% should be established whenever possible. Although
periodontal tissues, which increases the risk of periodontitis. recent research suggests that tetracycline antibiotics in
For example, higher AGE accumulation in periodontal combination with scaling and root planing may improve
tissues is associated with diabetes, and interactions between glycemic control, systemic antibiotics are not required
AGEs and their receptor (RAGE, the AGE receptor located routinely.
mostly on macrophages) result in activation of local
immunological and inflammatory responses. Increased C. CARDIOVASCULAR DISEASES
release of cytokines such IL-1, TNF-, and IL-6, increased There are four proposed mechanisms that suggest
oxidative stress, and disruption of the RANKL/OPG axis Periodontal disease is a risk factor for atherosclerosis. [15]
favour bone resorption as a result of these upregulated  The 1stis that periodontal pathogens or its components
responses. All of these factors cause local tissue injury, enter the bloodstream directly. Pathogenic bacteria in
accelerated breakdown of periodontal connective tissues, and periodontal tissues, particularly Gram-negative bacteria
alveolar bone resorption, resulting in periodontitis (P. gingivalis), enter the bloodstream and cause
aggravation. bacteremia. LPS and other Gram-negative bacteria
products cause systemic inflammation, which then acts
When looking at the relationship in the opposite directly or indirectly on the arterial walls, causing
direction, i.e., the impact of periodontitis on diabetes, the endothelial dysfunction.
proposed mechanism is that periodontal bacteria and their  The 2nd is to induce systemic inflammatory response.
products, along with inflammatory cytokines and other Periodontal inflammation can increase the levels of
mediators produced locally in inflamed periodontal tissues, cytokines in blood, including IL-1, IL-6, and TNF-a,
enter the circulation and contribute to upregulated systemic and then lead to the production of intrahepatic
inflammation. This results in decreased insulin signalling and inflammatory mediators such as CRP, which causes
insulin resistance, resulting in diabetes aggravation. systemic inflammation, damage endothelial cells and
Increased HbA1c levels, in turn, increase the risk of diabetes lead to formation of arterial plaques.
complications (including periodontitis), producing a  The 3rd is to trigger a systematic immunoreaction. Since
bidirectional, two-way link between the diseases.[14] heat shock proteins (HSP) of bacteria and humans are
very similar in structure, the cross-reaction is easy to
take place between HSP60 of P. gingivalis and humans.

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Volume 7, Issue 3, March – 2022 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
The over-expression of HSP60 of P. gingivalis can produce more inflammatory cytokines, and hence play a key
result in the damage of endothelial cells and then role in the onset of periodontal disease.
promote cellular immunologic response of plaques
which will induce inflammation of the plaques.  Management
 The 4th is to influence lipid metabolism. The oxidation Dentists should be well-versed in metabolic syndrome and
and aggregation of low-density lipoprotein cholesterin related disorders' indications, symptoms, and diagnostic tests.
can be promoted by periodontal pathogenic bacteria It's critical to develop protocols that help individuals with
(LDL-C). metabolic illnesses manage and avoid oral diseases on an
individual basis. These must include more than just closely
Increased levels of inflammatory markers (such as monitoring obese patients for periodontal disease burst.
CRP, IL-6, and TNF-a) in moderate to severe periodontal Changes in lifestyle, including but not limited to weight loss
disease patients can promote endothelial cell destruction and and food and dietary supplement intake, should be considered
worsen angiosclerosis, raising the risk of hypertension. in protocols to assist diminish a hyper-responsive
Evidence suggested that the ROS might be an important inflammatory trait. To better reduce periodontal
contributor to both PD and hypertension because ROS inflammation, dentists should recommend overweight and
produced by neutrophil infiltration participate in the obese periodontal patients for weight-loss interventions such
destruction of periodontal tissues, and the imbalance of as dietary therapy, behavioural therapy, medication, and
oxidation-antioxidation in oral cavity could negatively affect surgical procedures.
oxidative status in the whole body.
E. STRESS
 Management Chronic and repeated exposure to stressors have the same
In collaboration with the patient and his physician, dental effect on periodontal tissues in as they do on other body
practitioners may be the first line of defence in the discovery systems.[17]
and referral of a patient with cardiovascular illness, an
uncontrolled disease status, or oral adverse drug reactions, Stress pathways to periodontal disease
and they play an important role in the prevention and a) Stress and the immune system
treatment of oral and systemic disease. Stress can affect the immune system in 3 different
ways i.e., through the neural and endocrine systems:
[18]
The following basic suggestions assist medical and
dental healthcare workers who work with individuals who  Through the autonomic nervous system path ways
have or are at risk of developing PD and CVD. [16]  Through the release of neuropeptides
 Through the release of hypothalamic and pituitary
Patients with moderate to severe PD should be hormones.
informed that they may be at a higher risk of developing
CVD than periodontally healthy adults, and PD patients who b) Stress and behavioral changes
have one or more CVD risk factors should seek medical Health impairing behaviour and periodontal diseases:
assessment if they have not done so in the previous year.  Neglected oral hygiene– increase plaque
 Medical and dental experts should work accumulation– gingival inflammation.
collaboratively to control common risk factors for PD  Cigarette smoking- impairs collagen synthesis and
and CVD in patients with both of these disorders, increases MMP 8 level
such as hyperlipidemia, hypertension, smoking, and  Alcohol consumption
metabolic syndrome in PD patients.
 Disturbed sleeping pattern – decrease in growth
 To manage plaque and gingivitis, standard treatment
hormone- impairs the tissue repair response.
should be provided, as well as oral hygiene
guidelines, such as the use of anti-plaque toothpaste,  Poor nutritional intake can result in impaired wound
mouth rinse, and interproximal cleaning healing.

D. OBESITY  Management
The biologic processes behind the link between obesity The use of stress biomarkers offers a way to adapt
and periodontitis are unknown, but adipose-derived periodontal treatment to individual patients based on more
cytokines and hormones play a vital role. complicated and objective risk factors. This will improve
treatment outcomes while also lowering periodontal treatment
Obesity causes a 60% infiltration of macrophages in costs.
adipose tissue. Adipocytes secrete bioactive compounds
termed adipokines, which operate as signalling molecules to One of the most common ways to estimate physiological
the liver, muscle, and endothelium both locally and stress is to look at cortisol levels. Circulating levels of IL-6,
systemically. TNF, CRP, and insulin-like growth factor are all extensively
used indicators of chronic stress. [19]
Classic hormones (e.g., TNF-), hormone-like proteins
(e.g., leptin, resistin), proteins involved in vascular The stress reduction protocol consists of techniques that,
hemostasis, and angiotensin play a variety of roles. These when applied alone or in combination, reduce the amount of
adipocytokines stimulate monocytes, causing them to

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Volume 7, Issue 3, March – 2022 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
stress experienced by the patient during therapy, lowering based on the interactions between genetics, clinical, and
the level of risk. environmental factors that affect a person's health.

The Dental Office Stress Reduction Protocol includes V. DISCUSSION

the following steps:
 Recognize medical risk and worry. Through defining lifestyle, behavioral, and genetic
 Seek medical advice. factors, and how these interplay at the individual level to
 Medication in advance (Anti-anxiety or sedative- modify the clinical manifestation of the periodontal diseases,
hypnotic drugs given one night before the will become an intrinsic part of routine clinical practice.
appointment or one hour before appointment). However, before this can happen, we must first define our
 Scheduling of appointments. diagnostic, therapeutic, and long-term management goals in
 Reduced anxiety by reducing the amount of time terms of separate and measurable components, each of which
spent waiting. may then be tailored to the individual rather than the
 Monitoring vital signs: blood pressure, heart rate, population as a whole.
rhythm, and respiration rate
 Sedation by means of psychotherapy. Individualizing periodontitis risk is a critical necessity
for progress in the field of periodontitis. We have achieved
IV. GENETIC BASIS OF PERIODONTITIS significant advances in our understanding as a result of
remarkable discoveries and efforts by investigators and
Individual genetic diversity is responsible for a large physicians all around the world, but we now need to move
portion of the variation seen in the development of beyond retrospective observations and associations.
periodontal diseases. [20]
The only way to move forward in a procedure that may
Identification of probable genetic variations associated differentiate the value of periodontal specialist treatment is to
to various phenotypes and features of periodontitis, as well stratify patients in short-term challenge models and long-
as identifying and devoting resources to individuals actually term intervention studies. To demonstrate usefulness in
at risk of developing oral issues, rather than treating reducing local oral complications of periodontitis and
everyone as if they all have the same risk and disease assisting the management of chronic systemic diseases, we
experience. Family studies, twin studies, population studies, must identify complex situations that require alternative
and single nucleotide polymorphisms have all been used to preventative and therapy procedures.
examine the genetic basis of periodontal disease.
Periodontitis and IL-1 and TNF-alpha gene polymorphisms VI. CONCLUSION
have been thoroughly examined, and a favourable
association between periodontitis and these polymorphisms Personalized periodontics has the potential to change
has been shown. the way we think about, research, and practise
periodontology. Early breakthroughs in diagnostic and
Epigenetics is the study of alterations in gene regulation prognostic testing employing noninvasive samples such as
not caused by changes in the DNA sequence. It is the link saliva and gingival fluid have been encouraging. These could
between environment and phenotype. Epigenetic aid in determining who would develop periodontitis as a
modifications involve result of gingivitis. Periodontal health can be achieved
 DNA methylation, simply by practising good daily plaque control and refraining
from smoking, but high-cost, cutting-edge scientific
 Histone modification, and
breakthroughs in periodontics are critical. The most difficult
 gene regulation by non-coding RNAs. task will be to turn breakthrough technology, such as
Epigenetic modifications lead to the activation and personalized periodontics, into public-health-relevant
inactivation of a gene. Cancer and autoimmune or services that are available to everyone.
inflammatory illnesses, such as periodontitis, can arise as a
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