Periodontal medicine the updated version.pptx

Greetings from GSL Dental College, Rajahmundry

The current status of
periodontal medicine and its
relevance in dental practice
Dr Ashok K P
Prof & Head
Dept Of Periodontics
GSL Dental College
Rajahmundry

PERIODONTAL MEDICINE
Periodontal Medicine is a rapidly emerging branch of Periodontology,
focusing on the wealth of new data, establishing a strong relationship
between Periodontal Health or disease and systemic health or disease.
William and Offenbacher-2000

PERIODONTAL MEDICINE
Periodontal Medicine deals with a two way relationship in which
periodontal disease in an individual may be a powerful influence
on an individual’s systemic health or disease or the more
customarily understood role of systemic disease on influencing an
individual’s Periodontal Health or disease.
William and Offenbacher-2000

FOCAL INFECTION THEORY
• Focal Infection is an idea that a local infection affecting the
small area of the body can lead to subsequent infection or
symptoms in other parts of the body due either to the spread of
infectious agent itself or toxins produced by it.
Robert Koch

FOCAL INFECTION CHANGING CONCEPTS
• Hippocrates (460-370BC) – noted a case of rheumatism cured after
infected tooth extraction.
• Benjamin Rush (1745-1813) – recognized relation of oral infection to
general health.
• W.D.Miller (1853-1907) – proposed oral infections as the cause of
many diseases.

• William Hunter (1861-1937) – indicated dental diseases as a
cause of what he called “oral sepsis” – that caused
rheumatic & other chronic diseases.
• For major infections oral focus was the periodontium and
not periapical disease.
• G.V.Black – important role of dental profession in preserving
general health.
• Frank Billings, Edward C. Rosenow, Charles H. Mayo –
interested in the same concept.

• Cecil.R (1938) – no improvement in rheumatoid arthritis
patients after teeth extraction & tonsillectomy.
• Williams & Burkett – found no good scientific evidence to
support “focal infection theory”.
Many patients with diseases presumably caused by foci of
infection have not been relieved by removal of foci
Patients with same diseases may not have detectable foci of
infection
Foci of infection can occur in healthy persons with no ill effects.
Journal of the American Medical Association (1952)

SYSTEMS BIOLOGY
• It is the study of interaction between the components of
biological systems and how these interactions influence the
function and the behavior of that system.
Snoep et al-2005

SYSTEMS BIOLOGY
• The living systems are maintained by the continuous flow of matter and energy,
and thus any biological system will inevitably be a subsystem of a large one.
• The key feature of such a system is the interaction among the components.

Human organism is a single unit composed of seemingly infinite
number of biological processes so intertwined that abnormalities
of almost any of its parts or processes have profound effect on
multiple other body areas.
Vincent Friedwell and Kenneth Kornman (2009)

ASSOCIATION
Association is defined as the concurrence of two variables more often than
would be expected by chance.
CAUSALITY
Causality is defined as the relationship between an event (cause) and a second
event (effect) where the second event is understood as a consequence of the
first

Bradford Hill’s criteria (1971)
Strength of association
Biological gradient
Consistency of
the

RISK FACTOR
• Risk factor – distinctive characteristics/exposures that increase the
probability of disease outcome (Albandar, 2002).
• Is any characteristic, behavior, or exposure with a association to a particular
disease.
• The relationship is not necessarily causal in nature.
• It increases the risk of disease occurrence.
• It is verified to be associated with disease through longitudinal studies.
• eg: smoking and periodontal disease

Type of Study Ability to ‘prove’
causation
1) Randomised Controlled
Trial
STRONG
2) Cohort Study Moderate
3) Case-control study Moderate
4) Cross-sectional study WEAK
5) Ecological study WEAK
STUDY DESIGN
Relative ability of different types of study to ‘prove’
causation
NB: Assuming study well-designed & conducted & bias etc. minimised

Is Periodontitis unique ?
• Unusual anatomy of the tooth – The crown is exposed to
external environment, whereas the root is within the
connective tissues.
• Non-shedding outer layers of the tooth – facilitates diverse
microbial colonization held in proximity to soft tissues of
periodontium.
• Periodontitis is a Biofilm-induced disease – environment very
protective for colonizing organisms.
• Polymicrobial infection- Interplay of many putative organisms

Periodontitis disturbs systemic homeostasis
Chronic damage of epithelial tissues
due to periodontitis
may induce the periodontal pocket to
ulcerate that allows access to
the bloodstream
Bacteria and their toxins, cytokines,
mediators of inflammation
disrupt homeostasis when toxins gain entry
to the systemic circulation

IS PERIODONTITIS A RISK FACTOR FOR…….??
• Cardiovascular disease
• Diabetes mellitus
• Adverse pregnancy outcomes
• Respiratory infections
• Rheumatoid arthritis
• Osteoporosis
• Renal dysfunction
• Alzheimer’s disease

ADVERSE EFFECTS OF
PERIODONTAL DISEASE ON
CARDIOVASCULAR SYSTEM

PERIODONTAL DISEASE
Periodontal disease is an immuno
inflammatory disease initiated by micro-
organisms and characterized by the
destruction of the supporting tissues of the
tooth

CARDIO VASCULAR DISEASES
Cardiovascular diseases are the class
of diseases that involve the heart or
blood vessels. It refers to those
related to atherosclerosis (arterial
diseases)

CARDIO VASCULAR DISORDERS
• Endothelial Dysfunction
• Hyper tension
• Atherosclerosis
• Coronary heart disease
• Angina
• Myocardial Infarction
• Cerebro Vasclular Accidents
• Peripheral arterial disease

1. Endothelial dysfunction
2. Accumulation of foam cells
3. Inflammatory cells
4. Smooth muscle cells
5. Fibrous intima
6. Narrow lumen
PATHO PHYSIOLOGY OF CVD

Mechanism of Atheroma formation

• In 1989, Mattila & Colleagues found an increase in caries, Periodontal
disease, Pericoronitis in patients with recent MI when compared to
controls.
• Many Risk factors for MI were the same for Periodontitis, Mainly
• Smoking
• Older male patients
• Lower SES

Specific pathways linking Periodontitis
and CVD

Bacteria entering the circulation as
a result of periodontal infection,
dental procedures, and routine tooth
care result in varying levels of
bacteremia.
This may enhance the progression
of atherosclerotic cardiovascular
disease (red arrow).
Inflammatory mediators produced in
infected gingival tissues or as part
of the hepatic response to
periodontal infection may enhance
the progression of atherosclerotic
cardiovascular disease (blue arrow).
Dyslipidemia modulated by
periodontal infection primarily
affecting the hepatic response may
enhance the progression of
atherosclerotic cardiovascular
disease (green arrow).
Biological plausibility of the relationship between the development of athero-
thrombotic lesions and periodontal infection.

Periodontitis and atherosclerotic cardiovascular disease:
consensus report of the Joint EFP/AAP Workshop on
Periodontitis and Systemic Diseases.
“There is consistent and strong epidemiologic evidence that
periodontitis imparts increased risk for future cardiovascular disease;
While in vitro, animal and clinical studies do support the interaction
and biological mechanism, intervention trials to date are not
adequate to draw further conclusions.
Well-designed intervention trials on the impact of periodontal
treatment on prevention of ACVD hard clinical outcomes are needed.”
Tonetti MS, Van Dyke TE; working group 1 of the joint EFP/AAP workshop..
J Periodontol. 2013 Apr;84(4 Suppl):S24-9

Stroke/ Ischaemic Cerebral Infarction &
Periodontitis

Periodontitis as a risk factor for stroke

Indirect Systemic effects
• Elevated production of fibrinogen and CRP
Atheroma formation

Platelet aggregation
• Platelets selectively bind with some strains of
Streptococcus Sanguis and Porphyromonas Gingivalis.
• Aggregation of platelets is induced by Platelet aggregation
associated protein (PAAP) expressed on some strains of
these bacteria
• Thrombus formation
• Thromboembolism
• Stroke

• Association between periodontal disease
and stroke
George S. Sfyroeras, MD, PhD,a Nikolaos Roussas, MD,b Vassileios G.
Saleptsis, MD,b Christos Argyriou, MD,b and Athanasios D. Giannoukas, MSc,
MD, PhD, FEBVS,b Athens and Larissa, Greece
• Conclusions: There is evidence that periodontitis is
associated with increased risk of stroke. However, the
results of this meta-analysis should be interpreted with
caution because of the heterogeneity of the studies as
well as the differences in periodontitis definition. ( J
Vasc Surg 2012;55:1178-84)

EFFECT OF PERIODONTITIS ON
DIABETES MELLITUS

DIABETES
• Diabetes mellitus is a heterogeneous group of disorders
characterized by hyperglycaemia, absolute or relative insulin
deficiency or resistance to action of insulin.
• There is a two way relationship between diabetes and
periodontitis.

Effect of Diabetes on periodontium
Poor periodontal outcomes result from hyperglycemia
in diabetes due to changes in :
Host response
Blood vessels
Wound healing
Micro-
organisms

Change in oral Microorganisms
SALIVARY
FLUX
REDUCTION
HIGH
GLUCOSE
CONC IN
SALIVA & GCF
DEVELOPMENT OF
PERIODONTOGENIC FLORA
Thus susceptibility of diabetics to periodontal
disease is increased

Changes in Immune response
Function of neutrophils
and monocytes altered
Neutrophil
adherence,chemotaxis &
phagocytosis impaired.
Thus periodontitis is
aggravated
Monocytes &
Macrophages often
exhibit elevated
production of
inflammatory
mediators, and this
hyperesponsive state
increases host tissue
destruction

a)The fibroblast, does not function properly in high-
glucose environments.
b) The collagen produced by these fibroblasts is
susceptible to rapid degradation by MMP enzymes
which are elevated in diabetes.
Wound healing responses to chronic microbial insult
may be altered in those with sustained hyperglycemia,
resulting in increased bone loss and attachment loss.
Altered wound healing

Change in microvascular Integrity

Infection
Acute systemic
Endotoxemia
TNF-α +IL-β FFA, LDL,TRG
hyperlipidemia
Increased serum
pro-inflammatory cytokines
Diabetes
Altered lipid metabolism
Insulin
resistance
Monocyte
hyper response
Chronic localized Bacteremia
Effect of infection on glycemic control

Gram negative periodontal
infection
Increased insulin resistance
Worsened glycemic control Improved glycemic control
Improved insulin sensitivity
Periodontal treatment
Potential effects of periodontal infection and periodontal therapy on
glycemia in patients with diabetes.

MECHANISM BY WHICH PERIODONTAL
DISEASE MAY INFLUENCE DIABETES
1
• Acute Bacterial and Viral Infections
2
• Chronic gram -negative periodontal infections,
have significantly higher serum markers of
inflammation, such as CRP,IL6 and Fibrinogen
than subjects without periodontitis.
3
• Periodontal treatment may reduce inflammation
locally and also decrease the serum levels of the
inflammatory mediators,that cause insulin
resistance, thereby positively affecting glycemic
control

Diabetes and periodontal diseases: consensus report of
the Joint EFP/AAP Workshop on Periodontitis and
Systemic Diseases
Overall, there is consistent and robust evidence that severe periodontitis,
adversely affects blood glucose levels expressed as HbA1C in individuals with
and without diabetes.
Moderate-to-severe periodontitis is associated with an increased risk for the
development of diabetes. Evidence supports a dose-dependent
role for periodontitis and diabetes complications.”
• Chapple ILC, Genco R, and on behalf of working group 2 of the joint
EFP/AAPworkshop. Diabetes and periodontal diseases: consensus report of
the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin
Periodontol 2013;40 (Suppl. 14): S106–S112.

Guidelines
• Good glycemic control, an HbA1c value of less than 6% for most patients,
significantly reduces the risk for the serious complications of diabetes,
including periodontal disease.
• Treating periodontal infection in people with diabetes is an important
component in maintaining oral health. It may also play an important role in
establishing and maintaining glycemic control, and possibly in delaying the
onset or progression of diabetes and its complications.
•
• Therefore, dental health professionals might fulfill an important role in
maintaining or improving the health, and ultimately the quality of life, of
individuals with diabetes and GDM, as well as aiding in lessening the immense
burden of diabetes and periodontal diseases.

• When gum disease goes untreated in patients with diabetes, they are
put at greater risk for developing long-term complications associated
with diabetes, such as CVD and kidney disease.
• There is a great need for dental and medical practitioners to
communicate and partner to facilitate the care of patients with
diabetes. The physicians can assist in assessing if their patients are
being evaluated by oral healthcare providers, and if not, they should
make the appropriate referral.

Periodontitis and Adverse Pregnancy Outcome

For centuries. dental profession was aware of effect of pregnancy
on periodontal health.
In recent years due to the work of Offenbacher and associates, it
is realized that pregnancy and periodontal disease have a
bidirectional relationship and periodontitis can be a risk factor for
adverse pregnancy outcome

PERIODONTITIS & ADVERSE PREGNANCY OUTCOMES
• Preterm birth – one of the most complicated and challenging
issues in perinatal medicine
• Spontaneous preterm birth – social (maternal race/ethnicity,
poverty) and individual risk factors (underweight, tobacco use,
maternal infection).
• Periodontal disease occurs in 40% of pregnant women (Lieff et
al.,2004)

PRE-TERM BIRTH
LATE PRE-TERM BIRTH
birth <37wks gestational age
birth at 34-36wks gestational age
VERY PRE-TERM
(Martin et al.,2007)
Birth <32wks of gestational age
EXTREMELY PRE-TERM (Martin et
al.,2007)
Birth <28wks gestational age
LOW BIRTH WEIGHT (WHO 2005) <2500g
VERY LOW BIRTH WEIGHT (WHO
2005)
<1500g

Landmark study
• Greg Collins (1994) conducted series of experiments in
pregnant hamster animal model. Demonstrated that chronic
exposure to oral pathogens like Porphyromonas gingivalis in
a chamber model amplifies enhanced fetal-placental toxicity
of exposure during pregnancy.
• Offenbacher et al., (1996) (human study) conducted a case-
control study on 124 pregnant or postpartum women.
Significant association was observed between periodontal
disease and low birth weight.

Proposed hypothetical model of the association between periodontal disease and
adverse pregnancy outcomes (Ann Acad Med Singapore 2005)
Infection (bacterial vaginosis, Periodontitis)
Endotoxin/microbiological products
Inflammation
Pro-inflammatory mediator activation
IL-1,TNF-alpha,MMPs
Fetal toxicity
Pre-term low birth weight
Fetal growth restriction

Schematic summary of the effects of pro-inflammatory cytokine/matrix
metalloproteinases (MMPs) from periodontal tissues on pregnancy outcomes
(CRP = C reactive protein; GDM = gestational diabetes mellitus; IUGR = intrauterine growth
restriction; PGE2 = prostaglandin E ; PTB = preterm birth).

Effect of Periodontal
therapy on Adverse
Pregnancy outcome

Significant Effect of
Periodontal
Treatment on APO
No Significant Effect of
Periodontal treatment on APO
Lopez et al 2002,2005) Michalowicz et al., (2013)
Offenbacher et al., (2006) Alcione Maria Soares Dutra
Oliveira (2010)
Sadatmansouri et al., (2006)
Tarannum & Faizuddin (2007)
Nikolaos P Polyzos
(2010)
Jeffcoat et al (2003)

“Although periodontal therapy has been shown to be safe and leads to
improved periodontal conditions in pregnant women, case-related
periodontal therapy, with or without systemic antibiotics does not
reduce overall rates of pre-term birth and low birthweight.”
Sanz M, Kornman K; Working group 3 of joint EFP/AAP workshop. Periodontitis and adverse pregnancy
outcomes: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin
Periodontol. 2013 Apr;40 Suppl 14:S164-9.
Periodontitis and adverse pregnancy outcomes: consensus
report of the Joint EFP/AAP Workshop on Periodontitis and
Systemic Diseases.

PERIODONTAL DISEASE AND
PRE-ECLAMPSIA

Pre- eclampsia
• Pre- eclampsia is a maternal multi-organ disease that clinically
manifests in the second half of pregnancy by the appearance of
hyper-tension and protein urea.
Pre-Eclampsia is a disorder unique to pregnancy with prevalence of
2- 3%.
It is one of the leading cause of maternal morbidity and mortality in
the western world.
In recent years a number of studies have explored the relationships
between pre-eclampsia and periodontal disease.

Pathogenesis
• Pathogenesis of pre-eclampsia is not completely understood but it
is generally accepted that endothelial dysfunction of maternal
vascular system plays a key role in the clinical manifestation of
disease.
• It is believed that pre-eclampsia is most likely the result of
generalized inflammatory response including activation of
inflammatory and endothelial cells.
Saftlas et al-1990
Women with diseases associated with chronic low grade inflammation
such as diabetes mellitus, hypertension, obesity and arterial diseases are at
an increased risk of developing pre-eclampsia.
Rodie et al-2004

• The Periodontal disease is also associated with low grade
inflammation.
• It is hypothesized that patients with periodontal disease have an
increased risk of developing pre-eclampsia.

Systematic review on periodontal disease & pre-eclampsia
(Alina Kunnen et al.,2010)
• A generalized inflammatory response plays an important role in the
pathogenesis of pre-eclampsia; periodontal disease might contribute to
its pathogenesis.
• Questionable role of periodontal disease
• None of RCTs till date reported reductions in pre-eclamptic rate after
periodontal therapy during pregnancy.
• Larger RCTs – required to explore causuality and biologic mechanism.

Principles guiding dental treatment during pregnancy
• Women should be advised to seek oral health care prior to becoming pregnant and throughout
gestation.
• Oral health care is safe and effective during pregnancy
• First trimester diagnosis (including dental x-rays) is safe.
• Acute infection, abscess and conditions predisposing to bacteremia and sepsis require prompt
intervention regardless of the stage of pregnancy.
• Necessary treatment can be provided throughout pregnancy. However, the period between the
12th and 22nd weeks represents the best time to provide oral services, especially scaling and
root planning.
• Elective treatment for conditions considered not progressive may be deferred until after
delivery
• Delay in necessary treatment could result in significant risk to the mother and fetus

RESPIRATORY DISORDERS

• Pneumonia is the inflammation of lung tissues followed by the
accumulation of blood cells, fibrin & exudates in the alveoli
• COPD is characterized by chronic obstruction to airflow with
excess production of sputum resulting from chronic bronchitis
(CB) and or emphysema.
• Chronic bronchitis is defined as a condition associated with
excessive tracheo-bronchial mucus production to cause cough
with expectoration for at least 3 months of the year, for more
than 2 consecutive years.
• Emphysema is defined as the distention of the air spaces
distal to the terminal bronchiole with destruction of the
alveolar septa

• VAP – pneumonia developing in 48hrs or more after initiation of
mechanical ventilation
• HAP – pneumonia with an onset 48hrs or more after admission to the
hospital

• Scannapieco’s report (1992) – oral and/or periodontal infection may
increase the risk for bacterial pneumonia or COPD

Etiopathogenesis
• Four important mechanisms have been proposed to explain, how oral
bacteria can participate in the pathogenesis of respiratory infection.
• 1. Oral pathogens may be aspirated into the lung.
• 2. Enzymes in the saliva, which are associated with periodontal
disease, may modify mucosal surfaces to promote adhesion and
colonization by respiratory pathogens
• 3. Periodontal disease associated enzymes may destroy salivary
pellicles on pathogenic bacteria.
• 4. Cytokines released during periodontal disease process may alter
respiratory epithelium to promote infection by respiratory pathogens
Scannapieco FA ,Role of Oral Bacteria in Respiratory Infection, J Periodontol 70, 1999, 793-802 .

Aspiration of bacteria from oral cavity
Entry into upper airway & lungs
Failure of host defense to clear bacteria
Lung infection
VAP Bacteria adhere to endotracheal tube surface
Growth of biofilm
Biofilm dislodged & embolize distally to set up foci of infection

Systematic reviews
AUTHOR FINDING
Scannapieco et al., (2003) No sufficient evidence to say
there is an association between
periodontal disease and COPD
Azarpazhooh & Leake
(2006)
No sufficient evidence to say
there is an association between
periodontal disease and COPD

Periodontitis and systemic diseases: a
record of discussions of working group 4
of the Joint EFP/AAP Workshop on
Periodontitis and Systemic Diseases

COPD
• “An association with periodontitis is suggested based on analyses
of the NHANES data sets. There appears to be a dose effect,
whereby greater periodontal disease is associated with
increasing loss of lung function.
• The primary aetiological factor is smoking as modified by
underlying inflammation.
• Studies of the association between periodontal disease and
exacerbations of COPD would be valuable.”

Pneumonia
“The association between dental plaque and pneumonia appears to
be stronger than for plaque and COPD. The improved oral hygiene
reduces the risk of health care-associated pneumonia as
suggested by several meta-analyses. The relationship with
periodontitis however is not known.”
Linden JG ,Herzberg MC, Periodontitis and systemic diseases:a record of discussion of working group
4 of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases , J Periodontol , 84(4 suppl.),
2013, S20-3.

Guidelines
• 1. remove all dental appliances upon admission to the critical care unit
• 2. Conduct oral examination initially and daily by a nurse
• 3. Brush teeth two or three times per day; also floss if possible.
• 4. Rinse all oral surfaces with antimicrobial rinses.
• 5. Perform frequent deep suction of oral and pharyngeal secretions as needed,as well as
prior to repositioning the tube or deflating the cuff.
• 6. Remove hard deposits (e.g., tartar/ calculus) from the teeth, if possible.
• 7. Request that teeth be professionally cleaned before admission to the hospital for
elective procedures

Suggestions to health care providers
• 1.Place the patient’s head to the side or place in semi-reclined body
position.
• 2. Provide deep suction, as needed, in intubated patients to remove
oropharyngeal secretions that can migrate down the tube and settle
on top of the cuff.
• 3. Brush teeth using a wet soft toothbrush for approximately one to
two minutes.
• 4. Brush tongue and vestibular surfaces.
• 5. Apply mouth moisturizer inside mouth and lip balm if needed to
reduce risk of oral ulceration.

RHEUMATOID ARTHRITIS

• Rheumatoid arthritis is a chronic destructive inflammatory
disease characterized by the accumulation and persistence of an
inflammatory infiltrate in the synovial membrane that leads to
synovitis and the destruction of the joint architecture resulting
in impaired function.
• RA is a disabling condition, and can lead to long-term joint
damage resulting in persistent pain and loss of function in
affected areas

RHEUMATOID ARTHRITIS AND PERIODONTAL DISEASE
• The relationship between rheumatoid arthritis (RA) and the
progression of inflammatory conditions elsewhere in the body,
such as periodontitis, is controversial.
• While a number of studies have presented conflicting results
regarding a relationship between periodontitis and RA, there
have been recent reports suggesting a significant association
between these two common chronic inflammatory conditions.

A.. Clinical appearance of chronic periodontitis C. Clinical appearance of rheumatoid arthritis
B. Radiographic appearance of chronic periodontitis D. Radiographic appearance of
rheumatoid arthritis

• Clinically, this condition is characterized by joint swelling, joint
tenderness to palpation, morning stiffness, severe motion
impairment, progressive degeneration of synovial-lined joints, and
radiographic evidence of joint changes.

• Periodontitis has very similar cytokine profiles to RA,
consisting of persistent high levels of pro-inflammatory
cytokines, including IL-1β and tumor necrosis factor-alpha
(TNF-α), and low levels of cytokines which suppress the
immuno-inflammatory response such as IL-10 and transforming
growth factor- β (TGF-β).
• These cytokines, together with low levels of tissue inhibitors of
metalloproteinases(TIMPs) and high levels of MMPs and
prostaglandin E2 (PGE2), are associated with the active stages
of periodontitis.

• Periodontitis has very similar cytokine profiles to RA, consisting of persistent
high levels of pro-inflammatory cytokines, including IL-1β and tumor
necrosis factor-alpha (TNF-α), and low levels of cytokines which suppress
the immuno-inflammatory response such as IL-10 and transforming growth
factor- β (TGF-β).
• These cytokines, together with low levels of tissue inhibitors of
metalloproteinases(TIMPs) and high levels of MMPs and prostaglandin E2
(PGE2), are associated with the active stages of periodontitis.

• In both rheumatoid arthritis and periodontitis, inflammation is likely
initiated by antigen stimulation (in the form of peptide or virulence
factors), and the subsequent cascade of acute and chronic
inflammation leads to a vicious cycle of continuous release of pro-
inflammatory mediators perpetuated by the host’s own cells.
• Both the resident cells (synovial cells and keratinocytes in rheumatoid
arthritis, fibroblasts and osteoblasts in periodontitis) and the migrating
inflammatory cells are active players responsible for the destruction
observed in these two chronic inflammatory diseases

• Emerging evidence suggests a strong relationship between the
extent and severity of periodontal disease and RA. While this
relationship is unlikely to be causal, it is clear that individuals
with advanced RA are more likely to experience more
signiﬁcant periodontal problems compared to their non-RA
counterparts, and vice versa.
• Hence, the possibility exists that both conditions result from a
common underlying dysregulation of the host inﬂammatory
response.

• Reports of an epidemiological association with periodontal
disease, including the NHANES data set and case-control studies,
are inconsistent.
• Animal studies provide biological plausibility. (Kinloch et al.
2011).
• In human rheumatoid arthritis, antibodies against citrullinated
proteins and peptides are often detected in the blood reflecting the
enzymic conversion of arginine residues to citrulline in certain
proteins.
Periodontitis and systemic diseases: a record of discussions of working group
4 of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases

• Biological plausibility for an association with periodontitis is also
reflected in the detection of citrullinated proteins in inflamed gingiva,
which may be associated with elevated auto-antibodies to self-
antigens (Nesse et al 2012)

The Humoral Immune Response to Oral Bacteria Provides a
Stimulus for Development of Rheumatoid Arthritis
Periodontal infection
▼
Citrullination of proteins by P. gingivalis
▼
Production of autoantibodies to citrullinated proteins
▼
Cross reactivity with cartilage components
▼
Auto-immunity to self-antigens
▼
Rheumatoid arthritis

• While causality between the two diseases is very unlikely, the fact
that both diseases can impact each other is becoming apparent.
• Thus, it is proposed that these two diseases can exist as a
manifestation of generalized dysregulation of the immune and
inflammatory responses.
• Early evidence has suggested that treatment of periodontitis can
reduce the clinical symptoms of rheumatoid arthritis.
• Therefore, early intervention to prevent periodontal destruction
occurring in individuals with rheumatoid arthritis should be
considered

Periodontitis and Chronic Renal Disease

• CKD is associated with many physiologic changes that might
contribute to the development of periodontal disease.
• There are several documented physiologic changes in oral tissues that
have been associated with CKD. These include xerostomia, decreased
salivary pH levels, decreased mineralization,and loss of the lamina
dura.
• Additionally, some of the medications commonly prescribed to CKD
patients may increase the risk of developing periodontal disease

Effect of Periodontitis on CKD
• 1. Systemic inflammation due to periodontitis can affect the kidneys
• 2. Bacteria from plaque can invade the endothelium of kidney forming
atheromatous lesions, thus decreasing blood flow to the organ
• 3. CRP Levels ↑ and levels of albumin in blood↓
• The authors demonstrated that periodontal disease was associated with an
increased risk of all-cause death in CKD patients.
• Zhang, J., Jiang, H., Sun, M. et al. Association between periodontal disease and mortality in people with CKD: a
meta-analysis of cohort studies. BMC Nephrol 18, 269 (2017). https://doi.org/10.1186/s12882-017-0680-9
• Arsalan Wahid, Saima Chaudhry, Afifa Ehsan, Sidra Butt, Ayyaz Ali Khan
Bidirectional Relationship between Chronic Kidney Disease & Periodontal Disease . Pak J Med Sci. 2013 Jan-Mar;
29(1): 211–215

Periodontitis and systemic diseases: a record of discussions of
working group 4 of the Joint EFP/AAP Workshop on Periodontitis
and Systemic Diseases
• The association between chronic kidney disease (CKD) and
periodontitis in several studies is statistically significant and
consistent.
• Although hypertension and diabetes are the primary
aetiological factors, periodontitis is hypothesized to modify
both these aetiological factors and consequently the
presentation of CKD.

Treatment Guidelines
• A primary objective of periodontal therapy is the local elimination of Gram-
negative bacteria and their products. In patients with moderate to severe
periodontitis, decreased Gram-negative bacterial load through periodontal
therapy will also decrease systemic inflammation.
• Antibiotic prophylaxis before the dental appointment may be considered.
• Dental appointments should be scheduled the day after hemodialysis
sessions in view of the heparin used during hemodialysis.
• Among analgesics, postoperative use of acetaminophen is considered safe
but nonsteroidal anti- inflammatory drugs should be avoided.

Periodontitis and Alzheimer’s disease

• AD was named after Alois Alzheimer, a German psychiatrist and pathologist working in
Frankfurt.
• Alzheimer’s disease (AD) is one of the leading causes of dementia.
• Two types of AD are recognized. Early onset AD is present in less than 5 % of the
population and is genetically determined.
• Late onset or sporadic AD(LOAD) is the most prevalent type of AD and is believed to
result from the interaction of multiple genetic and environmental factors.
• The risk factors recognized are: cerebrovascular disease,hypertension, diabetes, obesity,
smoking, depression, psychological stress, and history of head trauma.
• Clinical features include loss of memory, difficulty in planning and executing tasks,
inability to recognize faces and orient objects, difficulty in communicating, and behavior
changes.

Pathogenesis of AD
• The pathologic hallmarks of AD are the presence of senile plaques,
neurofibrillary tangles, neuronal and synaptic dysfunction, and neuronal
loss. The senile plaques found in the brain parenchyma contain
extracellular aggregates of amyloid β-peptide (Aβ).
• Macroscopically, neuronal loss and brain atrophy occurs in several sites
including the hippocampus and temporal and parietal lobes resulting in the
thinning of the cortex and enlargement of the ventricles.
• The misfolded proteins hyperphosphorylated tau (ptau) and amyloid β (Aβ)
in the brain progressively sequester their native counterparts, leading to a
breakdown in neuronal structure and function.

Periodontal disease & Alzheimer’s -the connection?
• Bacteremia can occur during manipulations of the oral tissues and daily procedures
such as flossing,brushing and mastication particularly when periodontitis is present.
Under normal physiologic conditions, bacteremia lasts approximately 30 min until
cleared by the immune system.
• However, if the immune response is weakened, keystone pathogens such as P.
gingivalis and T. denticola can evade, subvert the immune system, and metastasize
at distant sites such as the brain and induce local inflammation.
• Several periodontal species can invade proximal tissue. By invading monocytes,
bacteria can use these cells as transport mechanisms to reach the brain.
• Riviere et al. detected six different periodontal treponemes in the brains in more
than 90 % of the 16 AD cases analyzed.

The influences of genetic, proteinaceous, environmental and inflammatory factors that may
contribute to the initiation and progression of Alzheimer disease (AD).

• Periodontal disease and the risk of Alzheimer’s disease and mild
cognitive impairment: a systematic review and meta-analysis.
• Xin HU,1 Jing ZHANG , 1 Yulan QIU1 and Zhaonan LIU 2021
• Thirteen eligible studies, of which eight reported AD (291 114
participants) and eight reported MCI (4805 participants), were
included in this meta-analysis.
• PD was related to an elevated risk of AD and cognitive impairment,
and that it should receive early intervention.

Management
• Currently, two groups of drugs are used, acetylcholinesterase inhibitors and
N-methyl-D-aspartate (NMDA) receptor antagonists. Acetylcholinesterase
inhibitors act by preventing acetylcholine degradation, thus increasing the
concentration of acetylcholine in the synaptic cleft and prolonging
cholinergic neurotransmission.
• N-methyl-D-aspartate (NMDA) receptor antagonists interfere with the
sustained activation of NMDA receptors thus facilitating neuronal function.
• Oral complications are not commonly encountered for acetylcholinesterase
inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists.
• Due to cognitive decline and associated functional deficits, dental plaque
control progressively deteriorates in those who have AD.

• Chronic stress is unpleasant, decreases performance and can lead to
mental and physical problems, the intensity of which depends on the
perception, processing and coping behaviour of the individual.
• stress has been shown to affect the hormones’ ability to regulate the
inflammatory response.
• In chronic stress conditions, under the effect of stress hormones such as
cortisol, there is simultaneous enhancement and suppression of the
immune system via alterations on cytokine secretion by T-helper (Th) 1 and
Th2 cells.

• In the late 1990s, Genco et al , in a cross-sectional study, reported
that stress associated with financial difficulties and poor coping
mechanisms, is a significant risk indicator for more severe
periodontitis.

SYSTEMIC DISEASES ASSOCIATED WITH PERIODONTAL
DISEASE
• Alzheimers disease
• Aneamia
• Atheroschlerosis
• Auto-immune disease
• Cancer
• Chronic obstructive pulmonary disease
• Colon cancer
• Crohns disease
• Death
• Dementia
• Diabetes
• Dry mouth
• Endometriosis
• Erectile dysfunction
• Fatigue
• Fever
• Fibromyalgia
• Gastro-oesophageal reflux disease
• Hypertension
• Infertility
• Inflammatory bowel disease
• Intellectual function
• Leukemia
• Low birth weight
• Lung cancer
• Lupus
• Metabolic syndrome
• Miscarriage
• Mouth cancer
• Multiple sclerosis
• Obesity
• Obstructive sleep apnea
• Osteoporosis
• Pneumonia
• Polycystic ovaries
• Pre-eclampsia
• Premature birth
• Psoriasis
• Renal disease
• Rheumatoid arthritis
• Stroke
• Stomach ulcers
Mark Bartold Editor, Australian Dental Journal ,2012

Conclusion
• Both dental and nondental healthcare practitioners, such as physicians, nurses, and
allied healthcare providers, share in the responsibility to educate the public
regarding the significance of oral health in achieving and sustaining whole-body
health.
• Although there is much that is still inconclusive about certain oral-systemic
relationships, there does exist sufficient evidence of the relationship between
periodontal disease and its role in amplifying systemic inflammation and increased
risk for heart disease, stroke, adverse pregnancy outcomes, complications of
diabetes, and increased risk for respiratory infections in institutionalized patients.
• Patients need to be counseled to provide information about oral health—especially
when gum disease has been diagnosed—to their other medical providers.

• Thanks to
Dr Meenu Merry C Paul
Principal,
Malabar Dental College

Dr Shabeer Ahamed
• Professor & Head
Dr Jeethu John Jerry
Professor Dr Hasbeena and Dr Ann

References
• 1. Periodontitis and systemic diseases Clinical evidence and biologic
plausibility. J Hirschfield and Ian LC Chapple 2021.
• 2. A Clinician’s guide to systemic effects of periodontal diseases by
Ronald C Craig And Angela Kramer
• 3. Periodontal disease and overall health A Clinician’s Guide by Robert
Genco
• 4. Oral signs of systemic disease by Nasim Fazel
• 5. Periodontics, Medicine, Surgery and Implants by Louis F Rose

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Editor's Notes