Periodontal medicine is an emerging branch of periodontology that focuses on relationship of periodontal health/ disease and systemic health/ disease.

1. Chitwan Medical College
&
Teaching Hospital

2. Department Of
Periodontics & Implant Dentistry
Guided By:
Prof. Dr. Fahrat Umer
Dr. Gauresh Kumar Patel
Dr. Shristi Kafle
Submitted by:
Binaya Subedi
BDS 4th Batch
College of Dental Sciences,CMC

3. Impact of Periodontal Disease on
Systemic Health

4. Contents
 Introduction
 Focal infection theory
 Periodontal disease and mortality
 Periodontal disease and Coronary heart disease
 Periodontal disease and stroke
 Periodontal disease and Diabetes
 Periodontal disease and pregnancy
 Periodontal disease and COPD
 Periodontal disease and Acute Respiratory Infections
 Conclusion
 References

5. Introduction
 The term “Periodontal Medicine” – first suggested by
Steven Offenbacher (1996)
“Rapidly emerging branch of periodontology focusing on
a strong relationship between periodontal health or
disease and systemic health or disease.”
- Steven Offenbacher (1996)

6. Historical Background
 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.

7.  William Hunter (1861-1937) – indicated dentistry as a
cause of what he called “oral sepsis” – that caused
rheumatic & other chronic diseases.

8.  Periodontal disease is an infectious disease but certain
systemic condition may affect the initiation and
progression of the condition.
 Evidence have shed light on converse side of the
relation
Systemic
Conditions
Periodontal
Disease

10. Focal Infection Theory Revised
 William Hunter (1900) first developed an idea that the
focal oral infections (eg; gingivitis, abscess) were
responsible for wide range of systemic conditions.
 He stated that, oral organisms had specific actions on
different tissues, acted by producing toxins, resulting into
low grade ‘subinfection’  produces systemic effects over
prolonged periods.
 Degree of systemic effects produced by oral sepsis depend
on the virulence of oral infection and individual degree of
resistance.

11. Subgingival Environment as
Reservoir of Bacteria
 Subgingival microbiota in patient with periodontitis
provides a significant and persistent Gram –ve
bacterial challenge .
Gram –ve
Organisms and
their products
mainly
LPS
Sulcular epithelium
Periodontal
Tissues and
Circulation
Bacteremia and
Septicemia

12.  Total surface area of pocket epithelium in contact with
subgingival bacteria and their products in a patient
with generalized moderate periodontitis is estimated
to be approx. size of palm of adult hand.
 Bacteremias are common after mechanical periodontal
therapy and also occurs frequently during normal daily
functions and oral hygiene procedures.
 Complete eradication of these bacteria is not possible
and their re-emergence is often rapid.

13. Periodontitis and Mortality
 Patients with poor periodontal health may also have
other risk factors that increases mortality rates.
 Host susceptibility factors that predispose the patients
to periodontitis also predispose them to systemic
conditions such as Ischemic heart disease, stroke,
respiratory infections etc.
May cause mortality if chronic low bacteremia persists

14. Periodontal Disease and Coronary
Heart Disease
 CHD and related events are a major cause of death.
 MI has been associated with acute systemic bacterial
and viral infections, and is sometimes preceded by
influenza like symptoms.
 Localized infections  chronic inflammatory reaction
has been suggested mechanism underlying CHD in
these individuals.

15.  Study done by Matilla et al found that MI patients had
significantly worse dental health than did the controls.
 This association between poor dental health and MI was
independent of the known risk factor for heart disease such
as age, hypertension, chlosterol levels, diabetes.
 Periodontal infection may affect the onset or progression of
atherosclerosis and CHD through certain mechanisms
increasing viscosity of blood, thrombus formation and
Embolization.

16. Factors affecting the blood viscosity:
Plasma fibrinogen
Plasma Lipoproteins (LDL/VLDL)
White Blood Count
Von Willebrand Factor
Increases blood viscosity
Increased viscosity of blood → increase risk of thrombus
formation → ischemic heart disease & cerebrovascular accident

17. Effect of Periodontal Infection
Ischemic Heart Disease
 IHD is associated with a process of atherogenesis and
thrombogenesis.

19. Systemic infections:

20. Daily Activities:
 The exposure time to bacteremia from routine daily
chewing and tooth brushing is much greater than from
dental procedures.
 An estimated 8% of all cases of infective endocarditis are
associated with periodontal or dental disease without a
preceding dental procedure.
 In periodontitis, periodontium acts as reservoir of LPS that
can readily pass into the circulation through the ulcerated
sulcular epithelium cardiovascular accidents.

21. Thrombogenesis
• Platelet aggregation plays a major role in
thrombogenesis .
• Most cases of acute myocardial infarction are
precipitated by thromboembolism
• Oral organisms may be involved in coronary
thrombogenesis i.e. S. sanguis & P. gingivalis

22. Thromboembolism mechanism
Oral pathogens– Streptococcus sanguis and P. gingivalis
Expression of -Plalelet Aggregation Associated Protein
on some of strains
Bacterial strains enters the circulation and aggregation of
platelets
Forms thromboemboli

23. Atherosclerosis
It is a focal thickening of the arterial intima , the innermost
layer lining the lumen of the vessel , and the arterial media,
the thick layer under the arterial intima consisting of smooth
muscle, collagen, and elastic fibers.
Intimal lesion is called atheroma or atheromatous or fibro
fatty plaques
Enlarges gradually, protrude into & obstruct vascular lumen

24.  Periodontitis & atherosclerosis have many potential
pathogenic mechanism in common
Both have
 Complex causation
 Genetic & gender predisposition
 Share many risk factors, most significant is smoking
status
 Periodontitis, which is a chronic inflammation
initiated by microbial plaque can predispose to
atherosclerosis.

25. LPS (Exotoxins) enter into circulation through ulcerated
and discontinuous sulcular epithelium
Adherence of monocytes to vascular endothelium through
ICAM-1, ELAM-1 & VCAM-1
Penetrate epithelium and migrate under the arterial
intima, ingest LDL in its oxidized state
Foam Cells
Atheromatous plaque

26. Once within the arterial media, monocytes  macrophages
Production of IL-1, TNF-α & PG-E2  propagation of
atheromatous plaque
Smooth muscle and collagen proliferation  thickening of
arterial walls
Decreased blood flow  microvascular accidents
Rupture of plaque  exposure of collagen and TF from
macrophages
Activation of platelet and coagulation pathways
accumulation of platelet and fibrin  thrombus formation
FGF, PDGF

27. Fig: Pathogenesis of Atherosclerosis

29. Role of Periodontal Disease in MI
or Stroke
Possible mechanism are;
 Effects of infectious agents in atheroma formation
 host mediated effects
 Common genetic predisposition for periodontal
disease & atherosclerosis
 Common risk factors such as life style

30. Effect of infectious agents
 Gram –ve bacteria & associated LPS causes infiltration of
inflammatory cells, prolifeation of arterial smooth muscle
and intravascular coagulation similar to atheroma
formation.
 Chronic Periodontal infection  chronic systemic
exposure  low grade bacteremia  host response
Alter coagulability, endothelial and vessel wall intergrity,
and platelet function
Atherogenic changes and Thromboembolic changes

31. Host Response to infection
 Patients with abnormally exuberant inflammatory response
often have hyperinflammatory monocyte/macrophage
phenotype
 They secret increased level of pro-inflammatory mediators
(IL-1, TNF-α, PG-E2) in response to LPS aggravated
response
 Patient with AP, Type-1 DM often have this type of
phenotype.

32. Common genetic predisposition
 This monocyte/macrophagae phenotype appears to be
under genetic and environmental control which are
intimately involved in pathogenesis of both
periodontitis and atherogenesis.
Common risk factors such as life style
 Diet induced elevation in LDL level upregulates the
monocyte/macrophage response to LPS destructive
and inflammatory cytokines increased risk of CHD
and increased periodontal distruction.
 Smoking is also risk factor for both.

33. Periodontal Disease and Stroke:
Presence of systemic infection
Production of Acute Phase Reactant proteins (CRP &
Fibrinogen)
Hypercoagulable state, decreased micro-cerebral
perfusion, increased risk of thromboembolism
Cerebral stroke
Greater ischemia & more severe post ischemic neurologic
defect.

35. Diabetes Mellitus
 Chronic hyperglycemic state due to relative and
absolute deficiency of insulin
 Hyposecrection of insulin or peripheral resistance of
insulin  impaired glucose uptake by the cells 
impaired glucose utilization  Chronic
Hyperglycemia
 Results into lipid and protein metabolism

36. Two Types:
 Type I Diabetes Mellitus (Insulin Dependent)
 Type II Diabetes Mellitus (Non- Insulin Dependent)
 Gestational Diabetes

37. Mechanism of Action of insulin
Ingestion of food
Secretion of insulin -ve Type I DM
Glucose uptake through glucose transpoters (GLUT-1 GLUT-4)
through insulin dependent process
-ve Type II DM
Utilization of blood glucose
Decreased blood glucose

38. Complications of Diabetes Mellitus
1. Retinopathy
2. Nephropathy
3. Neuropathy
4. Macrovascular disease
5. Altered Wound Healing
6. Periodontal Disease

39. Periodontitis and DM
 It is clear from epidemiological data that DM increases risk
and severity of periodontitis.
 The increased prevalence and severity of periodontitis
typically seen in patients with diabetes, especially those
with poor metabolic control led to the designation of
periodontal disease as sixth complication of diabetes (Loe
et al ).
 In diabetic patient with periodontitis, periodontal therapy
may have beneficial effects on glycemic control.

40. Effect of Periodontal infection on
Glycemia
 Acute viral and bacterial infection have been shown to
increase insulin resistance and aggravates glycemic control.
 Systemic infection increases tissue resistance to insulin,
preventing glucose from entering into the cell causing
elevated blood glucose level  required increased amount
of insulin to maintain normoglycemia.
 In type II DM, further insulin resistance induced by
infection exacerbate poor glycemic control
 In type I DM, normal doses of insulin may be inadequate to
maintain good glycemic control.

41. Periodontal infection/therapy and Diabetes

42.  Acute endotoxemia and cytokine production, mostly
TNF-α and IL-lß, induce insulin resistance and
decreased insulin action.
 TNF-α has been suggested as the mediator of insulin
resistance in infection by suppressing insulin induced
tyrosine phosphorylation (kinase) of insulin receptor
substrate-1 (IRS-1), thus impairing insulin action.

43.  Miller et al 1992, evaluated that scaling & root planing combined
with systemic doxycycline therapy for 2 weeks, when given in type I
diabetic patients with improved periodontal health also had
significant improvement in glycemic control.
 Treatment with scaling & root planing, surgery, selected tooth
extraction & systemic antibiotics resulted in decreased insulin
demand.
 Tetracycline can also be given as tetracycline is known to suppress
glycation of proteins & to decrease activity of tissue- degrading
enzymes such as MMPs.
 Diabetes is associated with greatly elevated production of
collagenase, low dose doxycycline has been used in treatment of
periodontitis in diabetic subjects.

45. Low Birth Weight
 Low birth weight infants are, as adopted by the
Twenty-ninth World Health Assembly in 1976 , infants
with birth weight of ‘‘less than 2500 g’.’
 They are 40 times more likely to die in neonatal period
than normal birth weight infants and account for two
thirds of neonatal death.
 Infants who survive  increased risk of congenital
anomalies, respiratory disorders and neuro
developmental disabilities.

46. Causes of LBW:
 Preterm labor or premature rupture of membranes (primary
cause)
 Smoking, alcohol or drugs use during pregnancy
 Inadequate prenatal care
 Race, low socioeconomic status
 Hypertension, diabetes
 High or low maternal age
 Genitourinary tract infection
 Maternal stress & genetic background
 Periodontal disease

47.  Labor is characterized by coordinated uterine contractions
leading to cervical dilatation, and finally expulsion of the
fetus.
 The earliest identified events in labor are increases in the
bioavailability of prostaglandin E2 , and in the concentration
of receptors for the hormone oxytocin.
 The increase in oxytocin receptors during labor induces the
stretching of the cervix and myometrium which is thought
to initiate a neurogenic reflex to the neurohypophysis of the
pituitary gland, which acts as positive feedback for oxytocin
production.
Preterm labor or premature rupture of
membranes

48. Remote Gram –ve infection (Periodontitis)
Exotoxaemia  Bacteria & products in amnion
Production of cytokines i.e. TNF-α, IL-1, IL-6, PG-E2 in
amnion
Increased amniotic Prostaglandins production, increased
expression of oxytoxin receptors and elevated oxytoxin
Pre-term contraction of uterus
Preterm labor

49.  Collins et al 1994, reported that P. gingivalis during
gestation causes significant increase in TNF- a &
PGE2.
 He also evaluated that there was decreased fetal birth
weight & increased fetal death after intravenous
injections with LPS derived from P. gingivalis.
 Offenbacher et al 1996 found that women having
LBW infants had greater clinical attachment loss than
women having NBW infants.

50.  Exposure to oral LPS down-regulates E-selectin
expression on endothelial cells  prevents the normal
leukocytic margination and diapedesis in response to a
secondary enteric LPS challenge.
 Increased possibility of systemic challenge with oral LPS
 may inhibit normal neutrophilic clearance of enteric
organisms  may permit a selective overgrowth or
invasion of Gram-negative organism within the
genitourinary tract may pose a potential threat to the
fetal-placental unit along with TNF-α & PG-E2 
growth retardation and fetal death.

51. Bacterial Vaginosis
 Caused by changes in the vaginal microflora in which
normally predominant facultative lactobacilli are replaced
by Gardnerella vaginalis, Prevotella, Bacteroides,
Peptostreptococcus, Porphyromonas, and others.
 It is a known risk factor for preterm labor, premature
rupture of membranes, and LBW.
 Women with preterm labor often have culture-positive
amniotic fluid, even in the absence of clinical infection. Of
culture-positive patients, the most commonly isolated
species is Fusobacterium nucleatum.

52. The primary mechanism has traditionally been thought
to be ascending infection from the vagina and cervix.
Direct tissue injury and induced release of
proinflammatory cytokines and prostaglandins
increased prostaglandin production and may result in
labor

54. Chronic obstructive Pulmonary
Disease
 Characterized by airflow obstruction resulting from
chronic bronchitis or emphysema.
 Emphysema is a chronic enlargement of airways distal
to bronchioles due to bronchiolar smooth muscles and
elastic fiber destruction.
 Chronic Bronchitis is narrowing of airways proximal to
distal bronchi due reactive hyperplasia of bronchial
mucos glands and hypertrophy of smooth muscles.

55. Risk factors of COPD:
 Cigarette smoking
 Industrial Smoke and tars
 Genetic conditions:
 Presence of defective alpha-1 antitrypsin
 Defective alpha-1 antichymotyrpsin
 Alpha-2 macroglobulin
 Vitamin D- binding protein

56. Effect of Periodontitis
 Share similar pathogenic process i.e mainly due to
exaggerated host response.
 Host inflammatory response mounted in response to
chronic challenge
 By bacteria in periodontal disease
 By factors like cigarette smoke in COPD

57. Neutrophil influx
release of oxidative & hydrolytic enzymes
Tissue destruction
Release of proinflammatory cytokines
Recruitment of monocytes & macrophages

58.  Hayes et al (1998) found a positive correlation
between advanced alveolar bone loss and COPD.
 Scannapieco et al 1998, individuals with poor oral
hygiene have been found to be at increased risk for
chronic respiratory diseases such as bronchitis &
emphysema

59. Acute Respiratory Infection
 The upper respiratory tract are often contaminated
with organisms derived from oral, nasal and
pharyngeal region.
 Pneumonia, is an infection of lungs parenchyma by
bacteria, virus, fungi and/or mycoplasma.
 It is broadly classified as:
 Community acquired pneumonia
 Hospital acquired pneumonia

60. Community Acquired Pneumonia
 Caused by Streptococcus pneumoniae & H.influenzae
in individuals hospitalized 90 days or before for 2 days
or more.
 Caused by:
 Inhalation of infectious aerosol
 Aspiration of oropharyngeal organism
 Till now no association between periodontal disease &
community acquired pneumonia has been found.

61. Hospital Acquired (nosocomial)
Pneumonia
 Gram- negative aerobic organism
 It is usually caused by the aspiration of oropharyngeal
contents during esophageal reflux containing Potential
Respiratory Pathogens (PRPs).
 PRPs may also originate in oral cavity, dental plaque serve
as a reservoir.
 Subgingival plaque harbor PRPs & periodontal pathogens,
associated with nosocomial pneumonia.

62.  Selective decontamination is a technique to eradicate
PRPs that combines
systemic antibiotics + orally administered nonabsorbable
antibiotics

63. Potential Mechanism Of Action
 Oral pathogens may be aspirated into lung to cause
infection.
 Periodontal disease- associated enzymes in saliva may
modify mucosal surfaces to promote adhesion &
colonization by respiratory pathogens.
 Cytokines originating from periodontal tissues may alter
respiratory epithelium to promote infection by respiratory
pathogens

64.  Scannapieco et al 2003, concluded that interventions
used to improve oral hygiene, such as mechanical
tooth brushing & chemical antimicrobials rinses, have
a potential to decrease the risk of nosocomial
pneumonia in high-risk patients, such as those in
intensive care units or those on ventilators.

65. Conclusion
 The periodontal medicine is an emerging field that offers
insight into the concept of oral cavity as on system
interconnected with the whole human body.
 Periodontal infection is a potential risk factor for a number
of systemic conditions. Fortunately, it is a modifiable risk
factor unlike age, sex and genetic factors.
 Periodontal disease may affect the host’s susceptibility to
systemic disease through sungingival plaque  acting as
reservoirs of Gram –ve bacteria  transient bacteremia 
release of microbial toxins & as a reservoir of inflammatory
mediators.

66.  Most of information available these days are based on
animal studies and the expanding concept of inter-
relationship between systemic health/disease and
periodontal health/disease may be further explored
for better understanding.

67. References:
1. Carranza’s Clinical Periodontology, 10th edition and
12th edition.
2. Essentials of Clinical Periodontology and
Periodontics, Shantipriya Reddy, 4th edition.

68. Past Questions

69. Thank You!!