Oral-systemic link has been termed Periodontal Medicine. Significance: Periodontal disease is preventable and readily treatable, thus providing many new opportunities for preventing and improving several systemic diseases. FOCAL INFECTION: Localized or Generalized infection caused by dissemination of microorganisms or toxic products from focus of infection. FOCUS OF INFECTION Confined area that (1) contains pathogenic microorganisms (2) can occur anywhere in body Diseases/Conditions affected by periodontitis A PREGNANCY, PREECLAMPSIA B ISCHEMIC HEART DISEASES, STROKE C DIABETES MELLITUS D PNEUMONIA, COPD E OSTEOPOROSIS F CANCER G ALZHEIMER’S DISEASE H. RHEUMATOID ARTHRITIS

1. PERIODONTAL
MEDICINE
1

3. Index
 Focal infection theory
 Diseases/Conditions affected by periodontitis
A PREGNANCY, PREECLAMPSIA
B ISCHEMIC HEART DISEASES, STROKE
C DIABETES MELLITUS
D PNEUMONIA, COPD
E OSTEOPOROSIS
F CANCER
G ALZHEIMER’S DISEASE
H. RHEUMATOID ARTHRITIS

4. The field of periodontal medicine addresses the following
question:
Is periodontal infection risk factor for systemic diseases that affect
human health ?
4

5. INTRODUCTION
 The emerging field of periodontal medicine offers new insights into the concept
of oral cavity as one system interconnected with whole human body.
 Evidence has shed light on the converse side of the relationship between
systemic health and oral health i.e. the potential effects of periodontal disease
on a wide range of organ systems.

6. “Oral health is not an independent entity cut off from the rest of
the body. Rather, it is woven deeply into the fabric of overall
health”
6

7. FOCUS OF INFECTION
Confined area that
(1) contains pathogenic
microorganisms
(2) can occur anywhere in body
FOCAL INFECTION: Localized
or Generalized infection caused
by dissemination of
microorganisms or toxic
products from focus of
infection.
7

8. FOCAL INFECTION THEORY
 In 1900 William Hunter, a British physician first developed the
idea that oral micro organisms were responsible for a wide range
of systemic conditions.
 According to this theory, he claimed restoration and extraction of
teeth with caries, pulpal necrosis and periapical abscesses to
eliminate the source of sepsis.

9.  He believed that the degree of systemic effect produced by oral
sepsis depended on the virulence of oral infection and
individual’s degree of resistance.
 For next 40 years, physicians & dentists believed that infections,
especially those originating in mouth, caused most of man’s
suffering & illness leading to extractions of infected teeth. That
era came to be known as era of focal infection

10.  The focal infection theory fell into disrepute in 1940’s and 1950’s
when wide spread extraction, often of entire dentition failed to
reduce the systemic diseases.
 Focal infection theory as proposed & defended in that period
was based on almost no evidence. Todays era of evidence based
medicine & dentistry provides an excellent environment to
examine possible relationship b/w oral infections & systemic
diseases.

11. Mechanism of interaction between periodontal
infection and systemic disorders
Subgingival environment act as reservoir of bacteria.
The subgingival microbiota in patients with periodontitis provides significant and persistent gram
negative bacterial challenge to host.
Production of products like lipopolysaccharide (LPS) occurs.
Periodontal tissue mount an immunoinflammatory response to bacteria.
Ready access of LPS, bacteria, immunoinflammatory cells from periodontal tissues to
circulation via sulcular epithelium occurs which is frequently ulcerated and discontinuous,
causing systemic manifestations.
Even with treatment, complete eradication of these organisms is difficult and their
reemergence is rapid.

12. Bacterial Plaque
Host Inflammatory Response, LPS
Systemic Diseases

13. MECHANISM OF ORAL FOCAL INFECTION
Metastasis of microorganisms
from an oral infected focus to
distant sites by either
hematogenous or lymphogenous
spread.
Metastasis of toxins or toxic
products through hematogenous
or lymphogenous spread (blood
stream or lymphatic channels)
from oral infected focus to distant
site where they may incite a
hypersensitive reaction in tissues.
13

14. ORAL INFECTION AND SYSTEMIC
DISEASE: A PARADIGM SHIFT
Adult human
body consists of
1013 somatic cells
& 1014 normal or
commensal
mirobes.
These commensal
bacteria reside on
surfaces of teeth
and/or prosthetic
implants within
complex ecosystems
termed “biofilms,” &
they reside on
surfaces of mucosal
epithelia that line oral
cavity, respiratory
tract, esophagus,
gastrointestinal tract &
urinary tract.
Under variety of
conditions, some of
these microorganisms
become opportunistic
& are associated with
local or systemic
infections, such as
Hemophilus influenza,
Streptococcus
pneumonia, Neisseria
meningitis &
Staphylococcus
aureus infection.
14

15. Oral microbial ecology is extremely sensitive to
potential insults that confront human hosts
throughout their lifespan.
One of best documented examples is involvement of
gram-positive Streptococcus sanguis &
Streptococcus oralis in infective endocarditis.
15

16. Diseases/conditions possibly influenced by
periodontal infection
A Reproductive system DISEASES
 Preterm low birth weight (LBW) infants
 Preeclampsia
B Cardiovascular system DISEASES
 Angina
 Myocardial infarction (MI)
 Cerebrovascular accident or Stroke
C Endocrine SysteM DISEASES
 Diabetes mellitus
D Respiratory SysteM DISEASES
 Chronic obstructive pulmonary disease (COPD)
 Acute bacterial pneumonia
E OSTEOPOROSIS
F CANCER
G ALZHEIMER’s DISEASE
h. Rheumatoid arthritis

17. PERIODONTITIS
& PREGNANCY
17

18. Periodontitis and Pregnancy
 Periodontal disease during pregnancy has been linked to
preterm low birth weight (PLBW) infants, early pregnancy loss,
and preeclampsia.

19. Preterm low birth weight (PLBW)
infants
 Periodontitis is a remote gram negative infection that may play role in PLBW
infants (PLBW < 2500gm)
 Premature and low-birth-weight (PLBW) infants are 40 times more likely to
die during the neonatal period. Such infants who survive the neonatal
period, face a higher risk of several neurodevelopment disturbances, health
problems (such as asthma, upper and lower respiratory infections and ear
infections) and congenital anomalies.

20.  Offenbacher and co-authors in 1996 from a case controlled study
suggested that women who delivered preterm low birth weight (PLBW)
infants had poorer periodontal health than mothers with normal birth
weight infants. They found the presence of higher levels
of Porphyromonas gingivalis, Bacteroides forsythus, Actinobacillus
actinomycetemcomitans and Treponema denticola organisms normally
associated with periodontal disease in mothers of PLBW babies as
compared to normal controls.

21.  In periodontal disease, transient bacteremia can occur leading to selective
colonization of undesired sites. Study by Han et al (2004) have shown that
hematogenous injection of orally related F. nucleatum in mice resulted in
preferential localization to placental blood vessels from which it crossed
the endothelium to the amniotic fluid and induced premature delivery and
stillbirths in a pattern similar to that seen in humans. This supports the
hypothesis that after transient bacteremia, oral bacteria like
F.nucleatum translocates to pregnant uterus and possibly to the fetus
hematogenously.

22.  Bacterial migration from periodontal tissues into blood circulation, also
stimulate the production of inflammatory mediators and increased
prostaglandin PGE2 production responsible for uterine contraction and the
onset of preterm delivery.
 F. nucleatum and P. gingivalis had been isolated from amniotic fluid and
cord blood in cases of preterm birth and neonatal sepsis by Gauthier S et
al (2011) and Katz J et al (2009) respectively.

23. Proposed mechanisms are-
 Translocation of the periodontal bacteria to fetoplacental unit
 Systemic dissemination of endotoxins on fetoplacental unit
 Systemic dissemination of inflammatory mediators (IL-1, IL-6, TNF-α,
PGE2) on fetoplacental unit.

24.  MECHANISM:
24Periodontal Infection
Bacteria & their products in
amnion
Inflammatory response with
cytokine production in
amnion
Increased amniotic
prostaglandin production
Preterm labour with
LBW infants

25. PREVENTION
 Hence periodontal disease appears to be an independent risk
factor for PLBW (preterm low birth weight infants) and there is
need to expand preventive measures by introducing oral health
programs as an integral component of prenatal care for
pregnant mothers.

26. Preeclampsia
 Preeclampsia is a pregnancy-specific disorder characterized by
increase in systolic arterial pressure (≥140 mmHg) and/or
diastolic pressure (≥90 mmHg) and proteinuria (≥300 mg/24 h),
after 20 weeks of gestation. It is dangerous for both mother and
fetus. Periodontitis is considered as a risk factor for it.
 Etiology: An increased systemic inflammatory response to pregnancy

27. Preeclampsia
 It is characterized by an abnormal vascular response to
placentation, manifesting as generalized vasospasm, activation
coagulation system and reduced organ perfusion affecting the
kidney, liver and brain.
 Periodontal disease burden pregnant women systemically with
endotoxins, inflammatory cytokines and oxidative stressors at
the maternal-fetal interface, thus acting as vascular stressor
that plays a role in development of Preeclampsia in pregnancy.

28.  Normal pregnancy is considered as mild pro-inflammatory state whereas
preeclampsia indicate more severe level of inflammation. The subgingival bacteria,
their products and pro-inflammatory cytokines may enter the bloodstream, reach
maternal–fetal interface, trigger/worsen maternal inflammatory response, increases
prostaglandin and cytokines levels in the plasma, causing complications in
pregnancy.

29. Prevention
 Maternal periodontal disease is a preventable disease in
contrast to preeclampsia, which can be treated but is difficult to
prevent. Hence, maternal periodontal disease must be taken as
an independent risk factor for adverse pregnancy outcomes
during evaluation of the pregnant women.

30.  The study by Jaiman G et al (2018) showed that birth weight of
newborn was significantly less in the preeclamptic group
suggesting that maternal preeclampsia could increase risk for
low birth weight infants.

31. PERIODONTITIS &
CARDIOVASCULAR
DISEASES
31

32. Periodontal Infection Links to Heart
Disease and Stroke
 Researchers have found that people with
periodontitis are almost twice as likely to
suffer from coronary artery disease.

33. Coronary Heart Disease
MECHANISM
Atherosclerosis Thromboembolism
Narrowing of
coronary arteries
Occlusion of
arteries by platelets
Myocardial ischaemia
Angina
Myocardial infarction

34. EFFECT OF PERIODONTAL INFECTION
Periodontal infection may affect the onset or
progression of Ischemic heart disease (Angina,
Myocardial infarction) through certain mechanisms.
1. INCREASED VISCOSITY
2. THROMOEMBOLISM
3. ATHEROSCLEROSIS

35. 1. Increased viscosity
Increased viscosity of blood may promote ischaemic heart disease by
increasing the risk of thrombus formation.
The factors promoting hypercoaguable state are:
Fibrinogen
White blood cell count
von Willebrand factor

36. INCREASE IN
Plasma fibrinogen
von Willebrand factor
White blood cell count
INCREASE
Blood viscosity

37. PERIODONTAL INFECTION
Fibrinogen levels and WBC counts are often increased in patients with
periodontal disease.
Individuals with poor oral health may also have significant elevations in
von Willebrand factor, increasing the risk of thrombus formation.
Thus periodontal infection may lead to increased risk for coronary
artery disease.

38. Periodontal infection
↑ Fibrinogen
↑ White blood cell count
↑ von Willebrand factor
↑ blood viscosity
Ischaemic heart disease

39. 2. THROMBOGENESIS
It is the process of formation of a solid mass in circulation from
the constituents of blood, the mass itself is called a thrombus.
Blood vessel wall can rupture and then get thrombus formed at
region of ulceration by aggregation of platelets.

40. Platelet aggregation plays a major role in thrombogenesis and most
cases of acute MI are precipitated by thromboembolism.
Oral organisms may be involved in thrombogenesis. Platelets
selectively bind some strains of Streptococcus sanguis, a common
component of supragingival plaque, and Porphyromonas gingivalis, a
pathogen mostly found in periodontitis.

41. Aggregation of platelets is induced by the platelet aggregation –
associated protein(PAAP) expressed on some strains of these bacteria.
PAAP –positive bacteria cause aggregation of circulating platelets,
resulting in formation of thromboemboli and thus coronary artery
disease.
Thus periodontitis associated bacteraemia with certain strains of
Streptococcus sanguis and Porphyromonas gingivalis may promote
acute thromboembolic events.

42. Sharma A et al in 2000 showed only P gingivalis expressed
virulence factors that can induce platelet aggregation.

43. 3. ATHEROSCLEROSIS
It is the focal thickening of the arterial intima,
the innermost lining of vessel lumen and the media,
the thick layer under the intima consisting of smooth
muscle, collagen and elastic fibres.

44. Early in the formation of atheromatous plaques, circulating
monocytes adhere to the vascular endothelium.
The adherence is mediated through several adhesion
molecules on endothelial cell surface, including intercellular
adhesion molecule-1(ICAM-1), endothelial leukocyte
adhesion molecule-1(ELAM-1), vascular cell adhesion
molecule-1(VCAM-1).

45. PATHOGENESIS OF ATHEROSCLEROSIS
Monocytes adhere to vascular endothelium. It penetrate into arterial media producing
proinflammatory cytokines and growth factors
Low Density Lipids (LDL) pass through damaged endothelium into blood vessel wall
Ingestion of oxidized low density lipoproteins(LDL) enlarges monocytes to form foam
cells.
Smooth muscle cell proliferation and atheromatous plaque formation thicken vessel wall
and narrow the lumen.

46. LDL’s are oxidized and then induce production of
bio-active molecules such as Interleukin 1,
Interleukin 6, Matrix Metalloproteases,
Prostaglandins, Platelet Derived Growth Factor,
Tumor Necrosis Factor Alpha.

47. Monocytes transform to macrophages and take up LDL
to form foam cells.
Monocytes trigger chronic inflammatory reaction with
lymphocytes and this results in tissue necrosis and fibrosis.
Blood vessel wall becomes distended and continues to
accumulate cholesterol, some areas become calcified.

48. Periodontal infection leads to production of several factors like LPS,
proinflammatory cytokines that upregulate the adhesion molecules,
which help in adherence of monocytes to vascular endothelium
After binding of monocytes they migrate under arterial intima.
Monocytes ingest low density lipoprotiens (LDL) and form foams cells
which are characteristics of atheromatous plaques

49. 
DNA from periodontal pathogens like Porphromonas gingivalis, Actinomyces
actinomycetemcomitans, Prevotella intermedia, T. forsythia had been
isolated from human atherosclerotic plaques. This suggested migration of
oral pathogens from oral cavity to distant sites. (Haraszthy VI et al; 2000)

50. Velsko IM et al in 2014 and Chukkapalli SS et al in 2014 showed
presence of Treponema denticola and P gingivalis in aortic
artherosclerosis of hyperlipidemic mice .

51. Periodontal infection
Gram-negative
bacteraemia/LPS
Endothelial damage
Platelet adhesion
Monocyte infiltration/proliferation
Cytokine /growth factor production
Thrombus formation
Atheroma formation
Vessel wall thickening
Thromboembolitic events

52. Direct effect
Direct effect Indirect effect
52
PERIODONTAL INFECTION
Monocytes
Macrophages
Liver
CRP, Fibrinogen, lipid
abnormalities, coagulating
factors
IL-1,IL-6
TNF-α
Vascular Lesion

53. STROKE
 People diagnosed with acute cerebrovascular ischemia
(in brain) were found more likely to have an oral
infection when compared to those in the control group.

54. Role of periodontal infection in
cerebral infarction or stroke
 Ischemic cerebral infarction or stroke is often preceded by systemic
bacterial or viral infection.
 Periodontitis is greater risk factor for stroke than smoking.
 Periodontal infection contribute by same three mechanisms
 atherosclerosis
 thromboembolism
 elevated production of fibrinogen and CRP

55. PERIODONTITIS &
DIABETES
55

56. Periodontal Infection and Diabetes
 Severe periodontal disease can increase blood sugar,
contributing to increased periods of time when the body
functions with a high blood sugar. This puts diabetics at
increased risk for diabetic complications. Thus, diabetics
who have periodontal disease should be treated to
eliminate the periodontal infection.

57. The Risk of Periodontal Disease
in Diabetics
 Anaerobic bacteria that live in the deep crevices and periodontal pockets,
get into the blood system and make it more difficult for a diabetic to control
their blood sugar. Additionally, the loss of teeth is a real problem for diabetics
since their support for a denture erodes away more rapidly (more bone loss)
than in the non-diabetic person. Diet and nutrition are usually compromised
with an undesirable increased intake of refined carbohydrates. Periodontal
disease increases the rate of C-Reactive Protein, which also causes
problems for diabetics and combines with elevations in blood sugar to
greatly increase the rate of heart attacks .

58. Role of periodontal infection in diabetes mellitus
 In Type 1 diabetes
The gram negative periodontal infection occurs
Increases in the insulin resistance of tissues preventing glucose from entering
targets cells
Causing elevated blood glucose levels
Requiring increased pancreatic insulin production to maintain normoglycemia
There is a poor glycemic control.

59.  In Type 2 diabetes
There is already significant insulin resistance
Further tissues resistance to insulin occurs induced by
gram negative infection
Worsened glycemic control

60.  Diabetes Prevention
 Bacteria living in the periodontal pockets
increase blood sugar, which would lead one to
suspect that people with periodontal disease
would be more likely to develop diabetes.

61. Treatment of
periodontitis in
uncontrolled diabetic
patients
ANTIMICROBIAL
THERAPY
(SCALING , ROOT
PLANING)
HOST MODULATING
AGENTS
(TO REDUCE
INFLAMMATORY HOST
PRODUCTS)

62. ANTIPROTEINASES
BONE SPARING DRUGS
ANTI INFLAMMATORY DRUGS
HOST MODULATORY AGENTS

63. ANTIPROTEINASES
SUBANTIMICROBIAL
DOSE OF
DOXYCYCLINE

64. ONLY DRUG
APPROVED BY
FDA TO BE
USED AS HOST
MODULATORY
AGENT

65. SUBANTIMICROBIAL DOSE OF
DOXYCYCLINE
Inhibit mammalian
collagenase (MMP-
8) activity with no
antibiotic resistance
inhibit MMP-13, so
decrease bone
resorption
Stimulates fibroblast
collagen production
Downregulates
expression of key
inflammatory
cytokines
(interleukin-1,
interleukin-6 and
tumour necrosis
factor-∝) and
prostaglandin E2
Scavenges and
inhibits production
of reactive oxygen
species produced by
neutrophils and
macrophages

66. Periostat
(20-mg doxycycline
hyclate, twice daily for
periods of 3–9 months
as an adjunct to
and root planing)

67. BONE SPARING
DRUGS
BISPHOSPHONATES

68. inhibit bone
resorption by
disrupting
osteoclast activity
increase
osteoblast
differentiation
bind to
hydroxyapatite
crystals and
prevent their
dissolution
BISPHOSPHONATES

69. Long term therapy
leads to
“bisphosphonate-
associated
osteonecrosis’’

71. Long term NSAIDS has shown
to cause gastroduodenal
problems, renal toxicity due
to COX-1 suppression
Beneficial effects of Omega-3
fatty acids, rh IL-11, TNF
antagonist on periodontitis in
diabetic patients have been yet
evaluated in animal studies
only.

72. PERIODONTITIS &
RESPIRATORY
DISEASES
72

73. Periodontal Infection and Respiratory Diseases
 Bacteria in our mouth can be aspirated into the
lungs to cause respiratory diseases such as
pneumonia, chronic obstructive pulmonary
disease (COPD) especially in people with
periodontal disease.

74. ORAL BACTERIA AS ETIOLOGIC AGENTS
OF RESPIRATORY INFECTION
 Variety of oral anaerobes & facultative species have been cultured
from infected lung fluids including P. gingivalis, Bacteroides gracilus,
Bacteroides oralis, Bacteroides buccae, Eikenella corrodens,
Fusobacterium nucleatum, A actinomycetemcomitans,
Peptostreptococcus, Clostridium. Most, if not all, of these organisms
have been implicated as etiologic agents in pathogenesis of
periodontal disease (Moore et al 1994).

75. ORAL BACTERIA AS ETIOLOGIC AGENTS
OF RESPIRATORY INFECTION
 Pneumonia is an important cause of morbidity and mortality in all
ages but more so in immunocompromised and older individuals.
 Periodontitis patients are three times more susceptible to
develop nosocomial pneumonia (Gomes-Filho IS et al in
2014)

76. ROLE OF PERIODONTAL INFECTION IN
RESPIRATORY DISEASE
 Bacterial respiratory infections are thought to be acquired through aspiration
(inhaling) of fine droplets from the mouth and throat into the lungs. These droplets
contain germs that can breed and multiply within the lungs to cause damage.
 Recent research suggests that bacteria found in the throat, as well as bacteria
found in the mouth, can be drawn into the lower respiratory tract. This can cause
infections or worsen existing lung conditions. People with respiratory diseases,
such as chronic obstructive pulmonary disease, typically suffer from reduced
protective systems, making it difficult to eliminate bacteria from the lungs.

77. Streptococci Viridans,
thought to be exclusively
benign members of oral
flora, may participate in
initiation and/or progression
of pneumonia.
C.Pneumoniae has been
causative agent for asthma,
bronchitis, COPD (Chronic
obstructive pulmonary
disease). In a mouse study
done by Yamaguchi H et al
(2006) he showed
translocation of this micro
organism from oral cavity to
lungs and then to spleen,
heart via monocytes.
Porto AN et al in 2016
showed P. gingivalis, A.
actinomycetemcomitans, T.
forsythia in orotracheal
intubation in toothed and
edentulous patients,
suggesting oral cavity even
without teeth, favors growth
of pathogenic
microorganisms
77

78. DENTAL PLAQUE AS RESERVOIR
OF RESPIRATORY PATHOGENS
Poor oral hygiene
results in an increase in
mass & complexity of
dental plaque, which
may foster bacterial
interactions b/w
indigenous plaque
bacteria &
acknowledged
respiratory pathogens
such as P. aeruginosa
& enteric bacilli.
These interactions may
result in colonization of
dental plaque by
respiratory pathogens.
Dental plaque may
therefore provide
reservoir for
colonization of
respiratory pathogens
that can be shed into
saliva.
Respiratory pathogens
are more likely to
colonize oral cavities of
patients with teeth or
dentures than
edentulous patients not
wearing dentures.
This finding suggests
that respiratory
pathogen colonization
is favored by presence
of nonshedding
surfaces and/or
conditioning of mucosal
surfaces by dental
plaque.
78

79. POTENTIAL MECHANISMS OF ACTION OF ORAL
BACTERIA IN PATHOGENESIS OF RESPIRATORY
INFECTION
(1) oral pathogens (such
as P. gingivalis, A.
actinomycetemcomitans)
may be aspirated into
lung to cause infection.
(2) periodontal disease–
associated enzymes in
saliva may modify
mucosal surfaces to
promote adhesion &
colonization by
respiratory pathogens.
(3) periodontal disease–
associated enzymes may
destroy salivary pellicles
on pathogenic bacteria.
(4) cytokines originating
from periodontal tissues
may alter respiratory
epithelium to promote
infection by respiratory
pathogens.
79

80. PERIODONTITIS &
OSTEOPOROSIS
80

81. OSTEOPOROSIS
Osteoporosis means literally
_porous bone, a condition
where there is too little bone to
provide mechanical support.
Osteopenia- reduction in bone
mineral density below than
what is required for mechanical
support.

82. Periodontal Infection and Osteoporosis
 Researchers have suggested that a link exists between osteoporosis
and bone loss in the jaw. Studies indicate that osteoporosis may lead
to tooth loss because the density of the bone that supports the teeth
may be decreased, which means the teeth no longer have a solid
foundation. However, hormone replacement therapy may offer some
protection.

83. Relationship between Periodontal disease and Osteoporosis
 Many studies have shown positive association
between osteoporosis and alveolar crest resorption.
 Fractures are very common in these patients
 Calcium and Vitamin D supplements have shown
positive impact on osteoporosis and periodontal
disease.

84.  Osteoporosis is frequently seen in women during
menopause due to decreased production of
estrogen. It causes suppression of calcium
absorption, increase in calcium excretion and
osteocyte apoptosis.
 Periodontitis in such patients release TNF-α that
induce collagenase activity, resulting in more bone
loss

85.  Harmone relacement therapy (HRT) is estrogen therapy that decrease osteoclast
formation and increase lifespan of osteoblasts and osteocytes. Dentist should refer to
medical practitioner for this.
 Nasal and subcutaneous calcitonin are available for postmenopausal osteoporosis.
Calcitonin is inhibitor of osteoclastic activity.
 HRT, Parathyroid harmone (PTH), Teriparatide improve osteoporosis and periodontal
regeneration
TREATMENT

86. PERIODONTITIS &
CANCER
86

87.  P. gingivalis and F. nucleatum directly interact with oral epithelial
cells and stimulate tumor progression in oral specific chemical
carcinogenesis model. (Binder Gallimidi A et al in 2015)
 P. gingivalis increases aggressiveness by promoting invasion and
metastasis of oral squamous cells via inducing pro-MMP9
expression in oral squamous cell carcinoma case. (Inaba H et al in
2014)

88.  Colorectal carcinoma is leading cause of death
nowadays. F. nucleatum has been shown to promote
pro-inflammatory microenvironment contributing to
neoplasia progression. (Yu YN et al in 2015)
 More studies are awaited to prove their relationship.

89. PERIODONTITIS &
ALZHEIMER
DISEASE
89

90.  Progressive neurodegenerative disease characterized
by progressive irreversible impairment of thinking,
memory, learning capacity, ending in death.
 Alzheimer disease and Periodontitis have bidirectional
relationship just as Diabetes mellitus and periodontitis.

91.  Increase in inflammatory cytokines are hallmark of both Alzheimer disease and
Periodontitis.
 Periodontitis release cytokines contributing to inflammation in brain, characterizing
Alzheimer disease.
 Studies conducted showing relationship between the two diseases are:
LPS from P. gingivalis and T. denticola ( Poole S et al in 2013);
Bacteria T. denticola (Ellen RP In 2005), C.pneumonia (Roulis E et al 2015)
have been isolated from postmortem human brains suffering from Alzheimer disease.

92.  Patients suffering from Alzheimer disease lose their
ability to maintain proper oral hygiene with
enhancement of risk of periodontitis. Also poor oral
hygiene causing periodontitis increase the risk of
Alzheimer disease.
 More studies are awaited to prove their relationship.

93. PERIODONTITIS &
RHEUMATOID
ARTHRITIS
93

94.  Autoimmune chronic inflammatory disease causing inflammation of
synovial membranes in joints.
 Anti-citrullinated protein antibodies are autoantibodies that are
unique of this disease.
 Its pathogenesis involve an enzyme that transforms arginine into
citrulline that causes posttranslational modifications in structural
proteins.

95.  In periodontitis P.gingivalis release deaminase that induce protein
citrullination. Chronic exposure of citrullinated proteins develop anti-
citrullinated protein antibodies (ACPA) that can aggravate disease
in RA patients. (Mikulis TR et al, 2014)
 Association between two diseases is not clear and more studies are
required.

96. Periodontal medicine in
clinical practice
 The concept of periodontal diseases as localized entities affecting only the teeth and supporting
apparatus is over simplified and in need of revision now.
 Rather than being confined to the periodontium, periodontal diseases may have wide ranging
systemic effects.
 Furthermore periodontal infection may exacerbate existing systemic disorders.
 Proper use of knowledge of potential relationship between periodontal disease and systemic
health requires the dentists to expand their horizons to step back from technically demanding
aspects of dental art and to recognize the oral cavity as one of many inter related organ systems.

97. Patient education
 Patient must be educated in disease prevention. Just as patient knows that
lowering cholesterol levels may decrease their risk for heart disease, prevention
of periodontal infection must also be emphasized.
 Controlling the risk factor of periodontal infection requires the dentist to
emphasize personal and professional preventive measures focused on thorough
oral hygiene and regular recall .