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.

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

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.

Pathways of Pulpal & Periradicular infection

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)

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

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

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.

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

Balance between Infection and Immunity Infection rate virulence factor Immunity Disease

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.

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.

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.

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

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

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

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.

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.

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

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