4. Focal infection
hypothesisBritish physician William Hunter,1900
• Oral micro-organism were responsible for a wide range of systemic conditions that were not easily
recognized as being infectious in nature
• By 1950s , the focal infection hypothesis fell from favor
FOCAL
INFECTION
CONTIGUOUS /
DISTANT
TISSUES
microorganisms
Toxic microbial
products
AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-20204/29/2020
5. Bacteria from dental plaque may enter the blood stream through discontinuities of the oral tissues
& travel through the blood to cause infection at distant site
Reservoir for Bacteria ≥ 500 species of
microbes
?
AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
Sub-gingival
microbiota
provides a
significant and
persistent gm-ve
challenge to the
host
4/29/2020
6. Periodontal disease and Mortality
• Studies support the association between poor oral health and an
increase risk for mortality
• Patients with more than 21% alveolar bone loss, the risk of dying was
found to be 70% higher than those without bone loss
AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-20204/29/2020
8. 1. Bacteria from our gums enter the saliva. From the saliva it may adhere to
water droplets within the air you inhale each time you breathe
Oral cavity to systemic
circulation
AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-20204/29/2020
9. 2. Bacteria associated with periodontal disease can enter the body’s
circulatory system through the gums (periodontium) around teeth and travel
to all parts of the body.
AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-20204/29/2020
10. 3.Inflammation associated with periodontal disease may stimulate a second
systemic inflammatory response within the body and contribute to or
complicate other disease entities that may have an inflammatory origin.
AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-20204/29/2020
11. Inflammatory
mediators(IL-1,IL-
6,TNF-ᾳ) IMMUNE RESPONSE
Periodonto pathogensPeriodontopathogens
or their products(LPS)
BACTEREMIA
Antibodies to
bacteria & to
cross-reactive
antigens such as
heat-shock
proteins, T-cells
sensitized
C-reactive protein, serum
amyloid ,fibrinogen
Bacteria induce
platelet aggregate,
invade endothelium,
digest matrix
PERIODONTAL INFLAMMATION
LIVER
TARGET ORGAN
AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-20204/29/2020
15. This a two way
street Periodontal
health /disease
Systemic health
/disease AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-20204/29/2020
16. SYSTEMIC DISEASE TO ORAL HEALTH
SYSTEMIC CONDITION S MAY HAVE EFFECT ON:
•Physiological response
•Vascular system
•Inflammotory response
•Immune system
•Tissue repair
AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-20204/29/2020
17. Thus in turn they modify
Susceptibility to disease
Plaque microbiota
Clinical presentation of periodontal disease
Disease progression
Response to treatment
Systemic conditions may alter host tissues and physiology, which
may impair host barrier integrity and host defense to periodontal
infection, resulting in more destructive disease.
AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-20204/29/2020
24. •Diabetic patient is more susceptible
to periodontal breakdown, which is characterized by
extensive bone loss, increased tooth mobility,
widening of periodontal ligament, suppuration and
abscess formation.
Pathogenesis
• There are several underlying factors that accompany
diabetes mellitus which may account for the apparent
increased prevalence of periodontal disease in this
condition. These factors are……………………
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
25. Vascular changes:- Changes include
thickening and hyalinization of vascular walls,
thickening of capillary basement membranes,
swelling and occasional proliferation of the endothelial cells,
splitting of capillary basement membrane.
Diabetic-induced changes in the capillary basement membrane may have an inhibitory effect on
the transport of oxygen, WBC, immune factors and waste products all of which could affect
tissue repair and regeneration.
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
26. Impairment of PMN function is a feature of diabetes mellitus.
Disorders include reduced phagocytosis and intracellular killing,
impaired adherence and impaired chemotactic response.
Suggested causes include inhibition of the glycolytic pathway with the PMNL’s abnormal cyclic
nucleotide metabolism, which disrupts the organization of microtubules and microfilaments, or a
reduction in leukocyte membrane receptors.
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
27. Biochemistry of crevicular fluid:- Alterations in the constituents and
flow rate of crevicular fluid have been shown to be associated with diabetes. Cyclic AMP
levels seems to be reduced in the diabetes group when compared with control.
Changes in plaque microflora:- Studies have indicated that
proteolytic activity has not been altered but hyaluronidase activity is lower in plaque from
diabetes.
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
30. What's the role of periodontal infection and /
inflammation in Diabetes status of person
?
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
31. • Evidence has consistently indicated that diabetes is a risk factor for increased severity of gingivitis and
periodontitis.
Conversely, periodontitis may be a risk factor for worsening glycemic control among patients
with diabetes and may increase the risk of diabetic complications. Periodontitis may initiate or propagate
insulin resistance in a manner similar to that of obesity, by enhancing activation of the overall systemic
immune response initiated by cytokines
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
32. • Proposed mechanism by which periodontal inflammatory mediators may contribute to the development of
insulin resistance in individuals with both type 2 diabetes and periodontitis.
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
33. The inflammatory mediators originating from periodontal sources can interact
systemically with lipids, free fatty acids and advanced glycation end products
(AGES), all of which are characteristic of diabetes.
PRRs = pattern-
recognition receptors
This interaction induces or perpetuates activation of the intracellular pathways, such as the I-kappa-B (IκB), I-kappa-B kinase-
β (IKKβ), nuclear factor-kappa B (NF-kβ) and the protein c-Jun N-terminal kinase (JNK) axes, all of which are associated with
insulin resistance
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
34. The activation of these inflammatory pathways in immune cells (monocytes or macrophages), endothelium
cells, adipocytes, hepatocytes and muscle cells promotes and contributes to an increase in the overall insulin
resistance, which makes it difficult to achieve metabolic control in patients with both type 2 diabetes and
periodontitis
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
36. •Given these mechanisms promoting insulin
resistance,
It seems that in individuals with type 2 diabetes and periodontitis, an
elevated chronic systemic inflammatory state induced by periodontal disease may
contribute to insulin resistance through a “feed-forward” mechanism, worsening
glycemic control.
Periodontitis may also contribute to the elevation of serum inflammation
mediators through enhanced in vitro production of TNF-α, IL-1β and PGE2 by
monocytes. This may indicate an innate hyper responsiveness of these monocytes to
periodontal bacterial challenge.
Periodontitis may also play a role through the translocation of gram-negative
species and their products from the periodontal biofilm into the circulation and
through direct cytokinemia from the gingival crevicular fluid (i.e., translocation of
cytokines from the periodontal space into the circulation).
Thus untreated Periodontal disease worsen the diabetes status of patient and vice versa
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020
37. • Key points
• People with poorly controlled diabetes (both type 1 and type 2
diabetes mellitus, both adults and children) must be considered at risk for
periodontitis, and people with diabetes should be informed of this risk.
• Early diagnosis and prevention are of fundamental importance to
avoid the largely irreversible tissue loss that occurs in periodontitis, and
early referral of adults and children with poorly controlled diabetes to dental
clinicians is indicated for periodontal screening.
• Periodontal therapy in patients with diabetes is associated with
improvements in glycaemic control (HbA1c reductions of approximately
0.4%) that may be clinically relevant in the management of diabetes.
• Oral health should be promoted in people with diabetes as an integral
component of their overall diabetes management. • Closer collaboration
between medical and dental clinical teams is necessary for the joint
management of people with diabetes and periodontitis, and contact with
dentists is important after the diagnosis of diabetes.
4/29/2020 AMU/BDS 3rd yr/ Prof Vivek /Perio/2019-2020 To be continue……………