Rationale of endodontic treatment

Contents
Pulpal & peri-radicular reaction to stimuli Inflammation Peri-radicular manifestations Endodontic implications

PULP & PERIRADICULAR TISSUES

Pulpal & peri-radicular reactions to stimuli

Damage to calcified structure of teeth and to the supporting tissues by noxious stimuli may cause changes in the pulp and the peri-radicular tissues Noxious stimuli can be either 1. Mechanical 2. Chemical 3. Bacterial

These stimuli produce either reversible or irreversible changes in the pulp and periradicular tissues depending on the following :1. Duration of stimulus 2. Intensity of stimulus 3. Pathogenicity of the stimulus 4. Host ability to resist the stimulus 5. Host ability to repair tissue damage

 Based on these grounds it can be comprehended that mild to moderate noxious stimuli to the pulp may produce following results:i. Sclerosis of the dentinal tubules ii. Formation of tertiary dentin iii.Cause reversible inflammation

 Irreversible inflammatory changes caused by severe injury lead to necrosis of the pulp & ensuing pathologic alterations in the peri-radicular tissues. As the pulp is enclosed in hard tissues with restricted portals of entry, it is organ of terminal and restricted circulation with no well organised collateral circulation Moreover there exist limited space to expand during inflammatory rxn.

Inflammation
Definition Causes Signs of inflammation Types of inflammation Inflammatory cells Mononuclear phagocyte system Reticuloendothelial system Vascular changes

Definition
It is defined as the local response of the living mammalian tissues to injury due to any agent Its a body defence rxn in order to eliminate or limit the spread of injurious agent as well as to remove the consequent necrosed cells and tissues.

Causes
Physical agents such as heat , cold , radiations and mechanical trauma Chemical agents such as inorganic or organic poisons Infective agents such as bacteria , viruses and their toxins Immunological agents such as cell mediated and antigen antibody rxns

Cardinal signs of inflammation

Signs of inflammation

Types of inflammation
Inflammation Acute
Transient Exudative PMNs Present Vasoactive amines,complement arachdonic acid derivatives (prostaglandins, leukotrienes)

Chronic
Persistent Proliferative Macrophages,lymphocytes, Plasma cells Absent/present if subacute Antibodies , lysosomal enymes, lymphokines

Stimuli

Type of reaction
Principal cells Pain Chemical mediators

Inflammatory cells

Differentiation of leucocytes

Inflammatory cells
MORPHOLOGY PMNs FEATURES Initial phagocytosis of bacteria & foreign body Acute inflammatory cell Bacterial phagocytosis Chronic inflammatory cell Regulate lymphocyte response MEDIATORS Primary, secondary & tertiary granules Reactive oxygen metbolites Acid & neutral hydrolysis Cationic protein Phospholipase Prostglandinds & leukotrienes IL-I B cells: antibody production T cells- delayed hypersenstivity, cytotoxicity

MONOCYTES/ MACROPHAGES

LYMPHOCYTES

Humoral & cell mediated immune response Chronic inflammatory cells Regulates macrophage response

Inflammatory cells
MORPHOLOGY PLASMA CELL FEATURES Derived from B cells Chronic inflammatory cells MEDIATORS Antibody synthesis Antibody secretion

EOSINOPHIL

Allergic states Parasitic infestations Chronic inflammatory cell

Reactive oxygen metabolites Lysosomal PGE2 synthesis

BASOPHIL/ MAST CELL Receptor for IgE Histamine molecules Leukotrienes Electron dense granules Platelet activating factor

Polymorphonuclear neutrophils
These cells along with eosinophils & basophils are called as granulocytes Granules contain proteases, myeloperoxidase, lysozyme, esterase, alkaline phosphatase, cationic proteins Diameter ranges from 10-15 m Comprise 40-70% of circulating WBCs Arise in the bone marrow from stem cells When number is increased in acute bacterial infections ,condition is called as neutrophilia

Functions
Initial phagocytosis of micro-organisms Engulfment of antigen antibody complexes Harmful effect of neutrophil is destruction of basement memberane of glomeruli and small blood vessels

Eosinophils
Larger than neutrophils but fewer in number Comprising 1-6% of total WBCs Granules are richer in myeloperoxidase and lack in lysozyme than neutrophils High levels steriods hormones lead to fall in number of eosinophils Absolute number is increased in following conditions 1. Allergic conditions 2. Parasitic infestations 3. Skin diseases 4. Malignant lymphomas

Basophils
Comprise 1% of circulating WBCs Contain basophilic granules in cytoplasm and polymorphonuclear nucleus Granules are laden with heparin and histamine They have receptors for IgE and degranulate when cross linked with antigen Role ;1. Immediate and delayed type of hypersensitivity rxn 2. Release of histamine by IgE sensitized basophils

Lymphocytes
20-45% of all WBCs Also present in spleen,thymus,lymph nodes & mucosa associated lymphoid tissue They have scanty cytoplasm & consist almost entirely of nucleus Functions :i. Antibody formation ii. Cell mediated immunity iii. In tissues they are dominant cells in chronic inflammation iv. In blood there number is increased in chronic infections like T.B & is ka as lymphocytosis

Plasma cells
Larger than lymphocytes with more abundant cytoplasm & an eccentric nucleus that has cart wheel pattern of chromatin Normally not seen in peripheral blood Developed from lymphocytes & rich in RNA & -globulin Most active antibody synthesis Number is increased in following i. Prolonged infection with immunological responses eg: syphilis ,TB, rheumatoid arthritis ii. Hypersensitivity states iii. Multiple myeloma

MONONUCLEAR-PHAGOCYTE SYSTEM &RETICULOENDOTHELIAL SYSTEM

This cell system includes cells derived from 2 sources: Blood monocytes:comprise of 4-8% circulating leukocytes.

Tissue macrophages in inflammation I. Macrophages in connective tissue II.Kupffer cells & macrophages of liver III.Alveolar macrophages in lungs IV.Macrophages of bone marrow V.Tingible body cells of germinal centers of lymph nodes VI.Littoral cells of splenic sinusoids VII.Osteoclast in bones VIII.Macrophages

IX. Microglial cells of brain X. Langerhans cells & dendritic histiocytes of skin XI. Hoffbauer cells of the placenta XII. Mesangial cells of glomerulus

Mononuclear phagocytes are scavenger cells of the body and also participate in immune system.

Role of macrophages in inflammation

Phagocytosis & pinocytosis Macrophages on activation by lymphokines released by T lymphocytes or by non Immunologic stimuli elaborate a variety of biologically active substances as under:a. Proteases such as collagenase & elastase that degrade collagen & elastic tissue b. Plasminogen activator activates the fibrinolytic system c. Products of complement d. Some coagulation factors that convert fibrinogen to fibrin e. Chemotactic agents for other leucocytes f. Metabolites of arachidonic acid g. Growth promoting factors for fibroblasts blood vessels & granulocytes h. Oxygen derived free radicals

Vascular changes
Injury , regardless of the cause or intensity, causes two fundamental vascular changes 1.Vasodilation 2.Increased capillary permeability A brief period of vasoconstriction is immediately followed by vasodilatation of the arterioles.

 This vasodilatation is accompanied by: 1. Increased rate of blood flow through vessels 2. Reduction in vascular reactivity 3. Decrease in the vascular flow resistance

Vascular response
Co-aggregation of RBCs Resistance for normal blood flow Loss of plasma leading to increased viscosity of the blood Reduction in oxygen saturation Increased carbon dioxide saturation Reduction in pH at the site of inflammation Prevention of removal of waste products Inflammation of adjoining normal tissues Partial followed by total necrosis

 The changes that help in repair and help return the vascular and tissue pressure back to normal are mainly of two types:1.The arterio-venous anastomoses that open in the pulpal vasculature in order to decrease the blood flow to the region of inflammation and by this method decreases vascular pressure 2.The increased tissue pressure allows the return of macromolecules and fluids to the venules.

Irritation to clinical crown(tooth preparation, caries)

Release of inflammatory mediators(BK,5-HT,PGs) Release of neuropeptides(SP & CGRP)

Localized pulpal inflammation Increased local tissue pressure Venous collapse Vascular stasis Ischaemia Local necrosis Circumferential vascular disturbance The vicious cycle of pulpal inflammation Necrosis of additional tissue

Total pulpitis

Increased tissue pressure

Release of intracellular inflammatory agents

PERIRADICULAR MANIFESTATIONS
After the necrotic process of the coronal pulp,the radicular root canals will serve as pathway to the periradicular area for noxious products of tissue necrosis & antigenic agents. These deleterious products induce bone resorption & granulation tissue in place of normal tissues.

 PERIRADICULAR PATHOLOGIC TISSUES CONTAIN:PMNS,LYMPHOCYTES,PLASMA CELLS ,MACROPHAGES,MAST CELLS,IMMUNOGLOBULINSIgG,IgA,IgM & COMPLEMENT. In the presence of inflammatory cells,anaphylactic,cytotoxic,antigen antibody & delayed hypersensitivity reactions occur.

TISSUE CHANGES SUBSEQUENT TO INFLAMMATION

1) Degenerative 2) Proliferative

Degenerative changes
Fibrous Resorptive Calcific Others : Suppuration Formation of pus

 Suppuration and formation of pus typically occurs following the release of proteolytic enzymes by injured or dying PMN cells These enzymes cause liquefaection of dead tissues and subsequent formation of pus The three requisites necessary for suppuration are: Inflammation followed by necrosis of tissue cells Substantial number of injured PMNS Digestion of dead tissues by proteolytic enzymes

Clinical relevance
For the devolpment of abscess microorganisms are not necessary Even in the absence of micro-organisms chemical and physical irritation can give rise to a sterile abscess.

Proliferative changes
Irritants that are sufficiently mild enough to perform as stimulants produce proliferative changes Clinical significance:- ability of any substance to act both as an irritant as well as stimulant Eg : calcium hydroxide which in high conc. And immediate proximity to a tissue would produce degenerative changes , however this material in low conc. And at periphery produce an opposite proliferative response hence the tissue response depends upon: Intensity of stimuli Proximity of tissue to stimuli

Endodontic implications
The presence of necrotic pulp tissue in the root canal results in diffusion of toxic material from necrosed tissue into and slightly beyond the area of pulpal and periodontal connective tissue Dr W.E Fish found 4 zones of reaction: Zone of infection/necrosis Zone of contamination Zone of irritation Zone of stimulation

Zone of infection/necrosis
Innermost or central zone of lesion Characterized by
Micro-organisms & their by-products PMNs

Zone of contamination
a.k.a exudative inflammatory zone Contains chronic round cells but no bacteria Cellular destruction is evident Bone cells are dead and undergo autolysis Lymphocytes are characterstic cells

Zone of irritation
a.k.a granulomatous zone or proliferative inflammatory zone Zone signifying the bodies attempt to repair macrophages Osteoclasts are characterstic cells Collagen network is not intact Signs of osteoclastic resorption of bone is evident

Zone of stimulation
a.k.a zone of endodontic capsulation or zone of productive fibrosis In this zone toxicity is reduced Characterized by fibroblasts and osteoblasts Collagen fibres are laid down by fibroblasts which both act as a wall of defence around the zone of irritation and a substrate on which future new bone formation would take place