1. Dr Gaurav Garg, Lecturer College of Dentistry, Al Zulfi, MU.
22/2/2015
Assalam Alekkum
Microbiology
&
Immunology
Dr Gaurav Garg, Lecturer
College of Dentistry, Al Zulfi, MU.

2. Learning Objectives At the end of lecture students should know:
Role of bacteria in Pulp & Periradicular diseases
Pathways of Pulpal & Periradicular infection
Flora of the Root canal & Periradicular lesion
Response of Pulp & Periradicular tissue to bacterial infection
Methods of control & eradication of root canal infection

3. Role of bacteria
The intact hard tissues of the tooth normally protect the pulp by acting as physical barriers to noxious irritants.
Causes of pulp/ periradicular disease can be physical, chemical and bacterial.
Bacteria cause predominately all pathoses of the pulp and the periradicular tissues.
To effectively treat endodontic infections, clinicians must recognize the cause and effect of microbial invasion of the dental pulp space and the surrounding periradicular tissues.

4. Pathways of Pulpal & Periradicular infection

5. ROUTES OF MICROORGANISM INGRESS
1. Through the
open cavity
2. Through the
dentinal tubules
3. Through
the gingival
sulcus & periodontal
Ligament
(through lateral canal)
4 Through extension
of a periapical
infection
from adjacent
infected
teeth
5. Through the
blood stream
(Anachoresis)

6. Flora of the root canal & periradicular lesion
Root canal infection is a mixed infection
85% to 98% of the bacteria are anaerobic.
The most frequently found anaerobic species are Bacteroides (Porphyromonas & Prevotella) and gram-positive anaerobic rods.
Acute symptoms are usually related to the presence of specific anaerobes, such as Porphyromonas gingivalis, Porphyromonas endodontalis, and Prevotella buccae.
A small percentage of facultative anaerobic bacteria are also present

7. Bacteria prevalent in endodontic infections
1. Anaerobic gram negative
Porphyromonas, Fusobacterium, Prevotella
2. Facultative gram negative
Neisseria, Capnocytophaga
3. Aerobic gram positive
Proprionibacterium, Peptostreptococcus
4. Facultative gram positive
Actinomyces, Streptococcus, Lactobacillus

8. Response of Pulp & Periradicular tissue to bacterial infection
Dental pulp and periradicular tissues react to bacterial infections as do other connective tissues elsewhere in the body.
The extent of damage as a result of bacterial penetration into these tissues depends on the virulence factors of participating bacteria and the resistance factor/ Immunity of the host tissues.

9. Balance between Infection and Immunity
Infection rate virulence factor
Immunity
No Disease

10. Balance between Infection and Immunity
Infection rate virulence factor
Immunity
Disease

11. Response of Pulp & Periradicular tissue to bacterial infection
The degree of pulpal and periradicular response to bacterial irritants varies from slight tissue inflammation to complete pulpal necrosis or acute periradicular osteomyelitis with systemic signs and symptoms of severe infection.

12. Response of Pulp & Periradicular tissue to bacterial infection
Direct exposure of pulpal tissue to microorganisms is not a prerequisite for pulpal response and inflammation.
As a result of the presence of microorganisms in the dentin, a variety of immunocompetent cells can be recruited to the dental pulp.
It is initially infiltrated by chronic inflammatory cells, such as macrophages, lymphocytes, and plasma cells.
The concentration of these cells increases as the decay progresses toward the pulp.
Polymorphonuclear leukocytes are the predominant cells at the site of pulp exposure.

13. Mild infections - do not result in significant changes in the pulp.
Moderate-to-severe infections
Release of inflammatory mediators (neuropeptides, vasoactive amines, kinins, complement components, arachidonic acid metabolites, and cytokines )
increased vascular permeability, vascular stasis, and migration of leukocytes.
lysosomal enzymes released from disintegrated leukocytes, can cause small abscesses and necrotic foci in the pulp.
Uncontrolled pulpal infection can result in total pulp necrosis and colonization of bacteria in the root canal system.
Egress of these organisms or their by-products from the root canal system into the periradicular tissues causes development of apical lesions.

14. Periapical inflammatory reactions are apparent in advance of total pulpal necrosis, when vital pulp is still present.

15. Periapical responses
to pulpal infection
Pulpal infections cause periapical tissue destruction, via stimulation of soluble host-derived mediators.

16. Periapical inflammation and bone destruction
Bacterial products
PMNs
IL-1, IL-6
TNFα
PGE MF
Periapical inflammation
and bone destruction L
IL-1
IL-2 + Ag B
IL-2

17. Methods of control & eradication of root canal infection
The steps involved in the disinfection of root canals are:
isolation of the involved teeth
Sanitation of the field of operation and use of sterile instruments
Removal of bacteria, their by-products, and debris
Prevent recontamination of the cleaned root canal
Obturation of the root canal in three dimensions
Placement of leak-resistant permanent restorations.

18. SYSTEMIC USE OF MEDICATIONS DURING ROOT CANAL THERAPY
Analgesics ( NSAIDS) and antibiotics are the major classes of medications used during the course of root canal treatment.
Antibiotics are indicated only if there is diffuse, rapidly spreading infection (cellulitis), fever & lymphadenopathy.
Because of the nature of root canal flora, however, no single antibiotic is always effective against all root canal infections.
Penicillin remains the antibiotic of choice because it is effective against most bacteria found in infected root canals.
In case of allergy, erythromycin is the drug of second choice.
Cleomycin produces a high concentration of this substance in the bone and is effective against anaerobic bacteria, it could be used as an alternative.

19. References Principal & Practice of Endodontics; Torabinezad
Textbook of Endodontics; Franklin S. Weine
Endodontics; Ingle & Bakland

20. Thank you!