periodontal medicine.pptx

PRESENTED BY :
SAHIL SHARMA
MDS STUDENT
2

⦁ Offenbacher 1996 defines periodontal medicine as a
rapidly emerging branch of periodontology which
focuses on the research of new data establishing a
strong relationship between periodontal health or
disease and systemic health or disease.
3

⦁ This means a two-way relationship in which periodontal disease in
an individual may have a powerful influence on an individual’s
systemic health or disease .
⦁ Non specific accumulation of bacterial plaque was once thought to
be the cause of periodontal destruction, but now it is recognised
that periodontitis is an infectious disease associated with
predominantly gram negative bacteria.
⦁ Although pathogenic bacteria are necessary for periodontal
disease, they are not sufficient alone to cause the disease. A
susceptible host is also required.
4

⦁ There are many systemic conditions that can
modify the host susceptibility to periodontitis.
⦁ Patients with immune suppression may not be able
to mount effective host response to subgingival
microorganisms, resulting in more rapid and severe
attachment loss.
5

⦁ Although the potential impact of many systemic
conditions on the periodontium is well documented,
recent studies done by Seymour et al suggest that
periodontal infection may significantly enhance the risk
for certain systemic condition or alter the course of
systemic condition.
6

⦁ Acc. To William Hunter in 1900,
◦ Oral microorganism- responsible for systemic
conditions
◦ Restoration instead of extraction, trapping of
infectious agents
◦ Gingivitis & periodontitis- foci of infection
Connection between oral sepsis & resulting systemic
condition could be shown by removal of causative sepsis
through extraction & observation of improvement in
systemic health
7

⦁ This theory fell into disrepute in 1940’s & 1950’s
when widespread extraction failed to reduce or
eliminate the systemic conditions to which the
supposedly infected dentition has been linked.
8

⦁ Cardiovascular/ cerebrovascular system
◦ Atherosclerosis
◦ Coronary heart disease (CHD)
◦ Angina
◦ Myocardial infarction (MI)
◦ Cerebrovascular accident (stroke)
⦁ Endocrine system
◦ Diabetes mellitus
9

⦁ Reproductive system
◦ Preterm low birth weight infants
◦ Preeclampsia
⦁ Respiratory system
◦ Chronic obstructive pulmonary disease
◦ Acute bacterial pneumonia
10

⦁ Well known relationship
⦁ 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.
⦁ Malthaner et al also found an increased risk of angiographically
defined CAD in subjects showing greater attachment and bone loss.
⦁ However after adjusting for other risk factor for the CAD the
relationship between the periodontal status and CAD was no longer
significant.
11

⦁ Associated with atherogenesis & thrombogenesis
12

⦁ Increased viscosity of blood → increase risk of
thrombus formation → ischemic heart disease &
cerebrovascular accident
⦁ Factors affecting blood viscosity
◦ Plasma fibrinogen
◦ Plasma lipoproteins
◦ White blood cell count
◦ von Willebrand factor
◦ Increased plasma fibrinigen level is considered as
risk factor for cardiovascular disease (Lowe et al).
13

Systemic or periodontal infection
↑ Fibrinogen, ↑ White blood cell count
↑ von Willebrand factor
↑ Blood viscosity
Ischemic heart disease
14

Thrombogenesis
15
⦁ Platelet aggregation plays a major role in
thrombogenesis .
⦁ Most cases of acute myocardial
precipitated by thromboembolism
⦁ Oral organisms may be involved
thrombogenesis
infarction are
in coronary

Thromboembolism mechanism
16
Platelet binds – Streptococcus sanguis and P. gingivalis
↓
Platelet aggregation – Plalelet Aggregation Associated
Protein
↓
Bacterial strains enters the circulation
↓
Forms thromboemboli
↓
Cardiac & pulmonary changes

 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 fibres.
 Occur in large & medium sized elastic & muscular
arteries
 Intimal lesion is called atheroma or atheromatous or
fibro fatty plaques
 Protrude into & obstruct vascular lumina
17

 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.
18

LPS released from microorganisms within the
periodontal pocket- enter the diseased
periodontium.
Monocytes/ Macrophages adheres vascular
endothelium
Ingest circulating LDL & forms foam cell –
atheromatous plaque
Smooth muscle & collagen proliferation – arterial
wall thickening
Narrows lumen & ↓blood flow
19

Figure showing pathogenesis of atherosclerosis
20

Periodontal infection
Gram- negative bacteremia/ LPS
Endothelial damage,
Platelet adhesion/ aggregation
Monocyte infiltration/ proliferation
Cytokine/ growth factor production
Thrombus formation
Atheroma formation
Vessel wall thickening
Thromboembolic events
21

1. Direct effects of infectious agents in atheroma
formation
2. Indirect or host mediated effects triggered by
infection
3. Common genetic predisposition for periodontal
disease & atherosclerosis
4. Common risk factors such as life style

 Direct effects of infectious agents in
atheroma formation
Studies done by Tonetti M et al, 2007 show
Porphyromonas gingivalis is found in carotid and
coronary atheromas.
Deshpande and colleagues (1998) conducted a
study and concluded that P. gingivalis can invade
and may proliferate in the endothelial cells
Herzberg and Meyer (1996) showing that P.
gingivalis is able to induce aggregation of
platelets, which is thought to be associated with
thrombus formation.

Indirect
infection
or host mediated effects triggered by
Periodontitis induces an inflammatory response,
production of acute-phase proteins, such as C-reactive
protein and fibrinogen. C-reactive protein and
fibrinogen are independent risk factors for coronary
artery disease, hence if they are induced by
periodontal infection, this may help explain the link
between periodontal disease and heart disease.

 A recent study by Wu and colleagues (1999) using the
NHANES III database, found that C-reactive protein and
plasma fibrinogen were related to poor periodontal health,
which provides support for this hypothesis.

Common genetic predisposition for periodontal
disease & atherosclerosis
Beck JD and colleagues (1996) have provided
a model proposing that there is a genetically
determined hyper inflammatory macrophage
phenotype in periodontal disease, which
for
contributes to the susceptibility
atherosclerosis

Potential linkage mechanisms for periodontal disease &
myocardial infarction
Evidence for the role of inflammatory mediators
C-reactive protein (CRP)
Smooth muscle cells proximal to apoptotic cells in the
arterial plaque produce secretory type II phospholipase
which interacts with inverted phospholipid bilayer in the
membrane of an apoptotic cell, thus preparing a nidus for
CRP to bind.
CRP induces local proinflammatory cytokine production &
may bind complement either prior to tissue localisation or
in situ, thereby enhancing removal of dying cell.
Complement activation in turn may precipitate collateral
damage.
28

Tumor Necrosis Factor-α
TNF-α has been shown to increase the synthesis of
triglycerides in the liver and to inhibit lipoprotein
lipase.
This elevated levels of triglyceride rich
glycoproteins and decreased levels of high density
lipoprotein cholesterol has been associated with
coronary heart disease.
Also macrophages and smooth muscle cells
expressing TNF –α are present in atherosclerotic
plaques, suggesting its role in atherogenesis.
29

Fibrinogen
30
•Fibrinogen is an acute phase protein mainly
synthesized in the liver in response to IL-6.
•Fibrinogen levels increase during infections and
inflammatory conditions including Periodontitis.
•IL-1 is considered as one of the important mediators
in the pathogenesis of periodontal disease and both
fibrinogen and fibrin can stimulate production of IL-1β
and protein by binding to CD18 integrin receptors on
normal human monocytes.

ICAM-1 and VCAM-1
31
molecule-1(ICAM-1) and
Intercellular adhesion
vascular cell adhesion molecule-1 (VCAM-1) are
important in the firm endothelial cell attachment and
transendothelial migration of leucocytes, thus
playing a central role in leucocyte recruitment and
their function in inflammatory reactions.
These molecules act as modulators of cell to cell
interactions as activators of certain target cells and
possibly, even as neutrophil chemoattractants. These
soluble factors have been associated with various
inflammatory conditions.

Presence of systemic infection before stroke
↓
Greater ischemia & more severe post ischemic
neurologic defect.
Stroke patients with a preceding infection had a slightly
higher levels of plasma fibrinogen & CRP than those without
infection
32

⦁ Syrjagen et al 1989, found a statistically significant poor level of
oral health in patients with ischemic cerebral infarction as
compared to controls.
⦁ Grau & colleagues 1997, reported that poor dental status was
associated with cerebral ischemia.
⦁ Beck & colleagues 1996, provided first longitudinal data relating
stroke to oral infections. They found that high mean alveolar bone
loss was predictive of subsequent stroke.
33

⦁ Complex metabolic disorder characterised by chronic
hyperglycemia.
⦁ Diminished insulin secretion, impaired insulin action or
a combination of both result in the inability of
glucose to be transported from the bloodstream into
the tissues which in turn results in high blood glucose
level.
⦁ Alteration in lipid or protein metabolism
34

1. Type 1 diabetes (insulin dependent)
2. Type 2 diabetes (non insulin dependent)
3. Gestational diabetes
4. Others
◦ Genetic defects in beta cell function
◦ Genetic defects in insulin action
35

Food digestion
↓
↑ blood glucose
↓
↑ Insulin secretion
↓
⦁ Muscle increases uptake of glucose
⦁ Muscle & liver store glucose as glycogen
⦁ Liver prevents glycogen from breaking down into glucose
↓
↓ blood glucose
36

Type 1 diabetes Type 2 diabetes
Age of onset Generally < 30 years Generally in adult hood
Most common body type Thin or normal stature Obese
Race White African American,
American Indian
Family history Common More common
Rapidity of clinical onset Abrupt Slow
Pathogenesis Autoimmune beta cell
destruction
Insulin resistance, impaired
insulin secretion, increased
liver glucose production
Endogenous insulin
production
None Decreased, normal or
elevated
Susceptibility to
ketoacidosis
High Low
Treatment may include Diet, exercise, insulin Diet, exercise, oral agents,
insulin
37

⦁ It is clear from epidemiologic research that diabetes
increases risk for & severity of periodontal disease.
⦁ 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 ).
38

⦁ Complications of diabetes mellitus
1. Retinopathy
2. Nephropathy
3. Neuropathy
4. Macrovascular
disease
5. Altered wound
healing
6. Periodontal disease
39

⦁ Taylor et al conducted a study amongst type 2 diabetes
patients and concluded that severe periodontitis was
associated with significant worsening of the glycemic control
over time.
⦁ He concluded that individual with severe periodontitis at
baseline examination were associated with a greater
incidence of worsening glycemic control over a period of 2 to
4 years as compared to those without periodontitis at
baseline examination.
⦁ Macrovascular complications were also found to be more
amongst individual with severe periodontitis at baseline.
40

⦁ In diabetic patients with periodontitis, periodontal therapy
may have beneficial effect on glycemic control.
⦁ This is true for patients with with relatively poor glycemic
control and advanced periodontal destruction before
treatment.
⦁ Hiltunen et al conducted a study amongst 65 subjects with
type 1 diabetes and chronic periodontitis and found that
although there was overall improvement in periodontal health
after therapy , 35 % of subjects had an improvement in
glycemic control after therapy, 37 % had no significant
change and 28 % showed worsening of glycemic control.
41

Effects of periodontal infection on glycemia
42
•Bacterial infections decrease insulin-mediated glucose
uptake by skeletal muscle and produce whole-body insulin
resistance.
•Acute endotoxemia and cytokine production, mostly
TNF-α and IL-lß, induce insulin resistance and decreased
insulin action.
•The insulin receptor tyrosine kinase, and the action of
protein kinase C may, either individually or in combination,
mediate some of the insulin effects such as translocation
and activation of glucose-transporting proteins.

•TNF-α has been suggested as the mediator of
insulin resistance in infection by suppressing insulin
induced tyrosine phosphorylation of insulin receptor
substrate-1 (IRS-1), thus impairing insulin action.
43

Gram- negative
periodontal
infection
Increased
insulin
resistance
Worsened
glycemic
control
44

Periodontal
treatment
Improved
insulin
sensitivity
Improved
glycemic
control
Decreased inflammation
45

⦁ Treatment with scaling & root planing, surgery,
selected tooth extraction & systemic antibiotics
resulted in decreased insulin demand.
⦁ 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.
46

⦁ 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.
⦁ Al-Ghazi et al 2003 & Engerbretson et al 2003,
reported short term improvements in glycemic control
with combination therapy, whereas no change was seen
with mechanical therapy alone.
47

⦁ The international definition of low birth weight
adopted by the Twenty-ninth World Health Assembly
in 1976 is a birth weight of ‘‘less than 2500 g’’
⦁ Low birth weight can be as a result of both a short
gestational period and retarded intrauterine growth.
48

⦁ Causes
◦ Preterm labor or premature rupture of membranes
◦ 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
49

⦁ Labor is characterized by coordinated uterine
contractions leading to cervical dilatation, and finally
expulsion of the fetus.
⦁ In term (‘‘normal’’) labor, rupture of the membranes
occurs after initiation of contractions.
50

•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.
51

⦁ Remote gram- negative infection may play a role in
LBW infants
⦁ Periodontopathic organisms & their products may
mediate host cytokine production in target tissues.
⦁ Collins et al 1994, reported that P.gingivalis during
gestation causes significant increase in TNF- a &
PGE2.
52

⦁ Significant correlation between both TNF- a & PGE2
levels, as well as fetal death & growth retardation.
⦁ Collins et al 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.
53

⦁ In a cross sectional study, women having LBW infants
had significantly higher levels of A.A, Bacteroides
forsythus, P. gingivalis and Treponema denticola in
their subgingival plaque.
⦁ Lopez et al 2002 found that women who received
SRP before 28 weeks of gestation, followed by
prophylaxis every 2 weeks until parturition, had a
LBW rate of 1.8% as compare to women who did not
receive periodontal therapy who had LBW rate of
10.1%
54

•Periodontal infections, serve as reservoirs for Gram-
negative anaerobic organisms, lipopolysaccharide (LPS,
endotoxin), and inflammatory mediators.
•Exposure to oral LPS down-regulates E-selectin
expression on endothelial cells and thereby prevents the
normal leukocytic margination and diapedesis which would
occur in response to a secondary enteric LPS challenge.
•This raises the possibility that systemic challenge with
oral LPS may inhibit normal neutrophil clearance of
enteric organisms that may permit a selective
overgrowth or invasion of Gram-negative organism within
the genitourinary tract. including PGE2 and TNF-α, may
pose a potential threat to the fetal-placental unit.
55

Bacterial Vaginosis
56
Caused by changes in the vaginal microflora in which
normally predominant facultative lactobacilli are
replaced by Gardnerella vaginalis; anaerobic
organisms, including species of the genera Prevotella,
Bacteroides, Peptostreptococcus, Porphyromonas,
and others.
Bacterial vaginosis is a known risk factor for
preterm labor, premature rupture of membranes, and
LBW.
.

The primary mechanism has traditionally been thought
to be ascending infection from the vagina and
endocervix.
Endotoxin & bioactive enzymes by many organisms
associated with vaginosis may directly injure tissue, as
well as induce release of proinflammatory cytokines
and prostaglandins.
57

•Throughout normal gestation, amniotic prostaglandin levels
rise steadily until a sufficient threshold is reached that
induces labor and delivery.
•Maternal infection may cause increased prostaglandin
production and may result in labor- inducing levels being
•achieved before full gestation
•Various pro-inflammatory cytokines such as IL-1, IL-6, and
TNF α have been found in the amniotic fluid of women with
preterm labor.
•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.
58

⦁ Airflow obstruction resulting from chronic bronchitis
or emphysema.
⦁ Bronchial mucosal gland enlarge & inflammatory
process occurs in which neutrophils & mononuclear
inflammatory cells accumulate within the lung tissue.
59

⦁ Risk factors of COPD
◦ Cigarette smoking
◦ Genetic conditions
🞄 Presence of defective alpha-1 antitrypsin
🞄 Variant alpha-1 antichymotyrpsin
🞄 Alpha-2 macroglobulin
🞄 Vitamin D- binding protein
60

⦁ Share similar pathogenic process
⦁ Host inflammatory response mounted in response to
chronic challenge
◦ By bacteria in periodontal disease
◦ By factors like cigarette smoke in COPD
⦁ Neutrophil influx → release of oxidative & hydrolytic
enzymes → tissue destruction directly.
61

⦁ Recruitment of monocytes & macrophages leads to
further release of proinflammatory cytokines.
⦁ 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.
62

⦁ Infection of the lungs caused by
Bacteria
Viruses
Fungi
Mycoplasma
63

Pneumonia
Community
acquired
Hospital
acquired
64

⦁ Caused by
◦ Inhalation of infectious aerosol
◦ Aspiration of oropharyngeal organism
⦁ Streptococcus pneumoniae & H.influenzae
⦁ Antibiotic therapy is highly successful in resolution
of the cases of community acquired pneumonia.
⦁ Till now no association between periodontal disease &
community acquired pneumonia has been found
65

⦁ Nosocomial pneumonia
⦁ Gram- negative aerobic organism
⦁ Many cases by anaerobic bacteria, subgingival
environment
⦁ It is usually caused by the aspiration of
oropharyngeal contents, potential respiratory
pathogens (PRPs)
66

⦁ Selective decontamination to eradicate PRPs- systemic
antibiotics + orally administered nonabsorbable antibiotics
⦁ PRPs may also originate in oral cavity, dental plaque serve
as a reservoir
⦁ Subgingival plaque harbor PRPs & periodontal pathogens,
associated with nosocomial pneumonia.
67
⦁ Furthermore, anaerobic
pocket may serve as
respiratory diseases.
organisms from
a inoculum for
periodontal
suppurative

⦁ 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.
68

1. Oral pathogens 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
69

⦁ Periodontal disease may affect the host’s susceptibility to
systemic disease through subgingival biofilms, acting as
reservoirs of Gram negative bacteria, transient
bacteremia, release of microbial toxins & as a reservoir of
inflammatory mediators.
⦁ More research is needed to these systemic diseases, &
then develop appropriate interventions
⦁ More research is needed before recommendations can be
made to treat periodontal disease as a strategy to prevent
or treat CVD, diabetes mellitus, pre-term birth & other
adverse pregnancy outcomes & also respiratory diseases.
70

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