personalized periodontology

1. Introduction to
Personalized
Periodontology
By
Romissaa Aly
Assistant lecturer of Oral
Medicine, Periodontology,
Diagnosis and Dental Radiology
(Al-Azhar University)

2. 1
• The current
understanding is that
periodontitis is the
body’s immune response
to plaque, involving a
complex combination of
plaque composition,
genetic make-up, general
health, and lifestyle and
social influences.
2
• Despite its complex
pathogenesis and
progression,
periodontitis may be
prevented simply by
plaque removal

4. • Severe periodontitis is the
sixth most common chronic
inflammatory disease globally.
As periodontitis is usually
painless, many who have it are
unaware of it.When left
untreated, it can lead to
significant morbidity and
financial burden. Periodontitis
is an under-acknowledged and
important public health
problem
• McGuire & Nunn have
demonstrated the
impossibility of
predicting teeth or
sites that will
deteriorate
periodontally, even in
individuals who
respond sustainably to
clinicians’ exhortations
for good plaque
control and regular
maintenance visits.

9. 1
• Periodontal Risk Assessment was
developed to group patients based on
their average risk levels in order to aid
resource allocation and determine
recall intervals.
• However, the adoption of this tool in
the clinical setting has been limited
because its additional benefits for
patient management and treatment
remain unclear
2

10. 1
• The most cutting-edge research to
determine those at risk of
developing and progressing
periodontitis is occurring in the field
of personalized periodontics.
Simply put, it involves utilizing
biomarkers to predict periodontal
disease susceptibility, determine
optimal management and enhance
treatment outcomes

11. 1 2 3
• .This ‘personalized medicine’
approach is also known as stratified,
individualized and/or precision
medicine. The term was first coined
in the context of genetics but it now
broadly encompasses other
personalized information, such as
the molecular or cellular
components of health and disease.
4

16. it is considered that the immunophenotype plays an
important role in the severity of periodontitis, since it is
considered that individuals with an overreactive
genetic predisposition excessively react even to small
amounts of bacterial biofilms, and this is particularly
associated with periodontitis Stage 3 (previously
called severe periodontitis) affecting up to 20% of the
population

17. Standard treatment protocols often fails to
arrest progressive periodontal destruction as in
Stage 3 periodontitis, while such patients
exhibits low-grade systemic inflammation.

18. Precision medicine is based on a combination of
clinical parameters and biological markers reflecting
the underlying biological processes; this enables
highly reliable prediction of periodontal disease
susceptibility, early diagnosis, prognosis, and
planning of the most effective and safe treatment
strategy meeting individual patient needs.[

19. A biomarker is a substance used to indicate a
biologic state and is an objective measure to
evaluate the present and future disease activity.
Various biological media like saliva, serum and
gingival crevicular fluid are used to determine
biomarkers in periodontal health and disease.

20. A single biomarker will not able to predict
periodontal disease activity and severity. So
combinations of biomarkers are used to
predict the disease activity

27. Predictive markers are used before disease
occurrence for the identification of risk factors and
estimation of the overall patient risk, aiming at
adjustment of the screening protocol and related
modification of risk factors for optimal disease
prevention.
 For this purpose, static markers are usually used;
these do not change over time and are typically
genetic markers

28. From genetic point of view,
periodontitis arises as a result of
single nucleotide polymorphisms
(SNPs). Various studies explored role
of SNPs in periodontitis

29. • William Giannobile utilized personalized
medicine approach in his study in which he
evaluated tooth loss that is one of the
terminal outcome of untreated periodontal
disease in 5117 periodontitis patients, over a
period of 16-year.
Patients were stratified based on three risk
factors, which were smoking, diabetes and

30. • If patients had one or more of these
risk factors, the investigators classified
them as being at high-risk of
periodontitis, and at low risk if they
had none of the three risk factors.

31. SNPs in IL-1β, IL1RN, FcϒRIIIb, VDR and TLR4 genes
may underline susceptibility to more destructive forms
of periodontitis[26] while polymorphisms in the IL1β,
IL1RN, IL6, IL10,VDR,CD14,TLR4 and MMP1 genes
might be responsible for general susceptibility to
chronic periodontitis.[27]

32. Prognostic markers are measured when
disease occurs; they do not need to change
over time, and they serve to estimate disease
characteristics, stage, and grade, which are
indispensable for accurate prognostics of the
progression pattern and responsiveness to
different treatment protocols.

33. IL1A and IL1B genetic variations are significant
contributors to chronic periodontitis in
Caucasians.[29]
TNFα gene located on chromosome 6 within the
major histocompatibility complex (MHC) gene
cluster at the location 6p21.3 is associated with
familial ability to produce higher or lower cytokine
levels during periodontitis.

34. Diagnostic markers comprise a wide group of
indicators able to disclose disease onset,
disease activity, and related disease
progression, usually represented by fast-
response biochemical and microbiological
markers.

35. The inflammatory biomarkers in
periodontology are represented by pro- and
anti-inflammatory cytokines, host-derived
enzymes, and markers of oxidative stress.
they are preferably used to estimate disease
activity, progression, and compliance with
administered treatment.

36. Soft tissue markers are used for monitoring soft
tissue degradation and regeneration, and matrix
metalloproteinases (MMPs) and growth factors are
the most repurposed markers used in
periodontology.
Increased levels of MMP-8 are signifying
conversion of gingivitis into periodontitis

37. Host Genome, Epigenome, and Oral Microbiome Interactions: Toward Personalized
Periodontal Therapy
Journal of Periodontology, Volume: 84, Issue: 9, Pages: 1266-1271, First published: 01 September 2013, DOI:
(10.1902/jop.2012.120531)

38. Clinical application of a
personalized approach towards
the treatment of periodontitis.
GC – Gas chromatography; MS –
Mass spectrometry

39. Systematized approach to metabolomics analysis–from
processing to results

41. Limitations of personalized
medicine

42. • Limitations include the
use of genotype- guided
therapies that requires
clinicians to have a level
of knowledge sufficient to
understand and interpret
the rationale for
prescribing for certain

43. • Due to limited drug alternatives,
patients carrying gene variations
may be left without any alternatives for
treatment.
•
• Also, the need for alternative drugs that
serve only a small portion of the
population and the great cost of bringing
a new drug in market may be a
disincentive for drug companies

44. • In-vitro quantification of drug and
drug metabolites in blood sample
of a patient can be done through
liquid chromatography, mass
spectrometery, flow cytometery and
SPR biosensing.
• Using ELISA for applying
personalized medicine in regular
practice may not be really possible
as they are expensive, time-

48. F I G U R E 1 Principles and
application of periodontal
tissue bioengineering. A.
Components of periodontal
tissue engineering. Six
factors
constitute for successful
periodontal tissue
engineering: cells, signal,
scaffold, mechanical loading,
pathogen control and ideal
blood supply.

49. Image-based
scaffold design for alveolar bone
bioengineering