Rationale of Endodontic Treatment

Rationale of endodontic treatment

Contents

• Pulpal & peri-radicular reaction to stimuli

• Inflammation

• Peri-radicular manifestations

• Endodontic implications

PULP & PERI-RADICULAR 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 peri-radicular 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

• It’s 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 inflammationInflammation Acute Chronic

Stimuli Transient Persistent

Type of reaction Exudative Proliferative

Principal cells PMNs Macrophages,lymphocytes,Plasma cells

Pain Present Absent/present if subacute

Chemical mediators

Vasoactive amines,complement arachdonic acid derivatives (prostaglandins, leukotrienes)

Antibodies , lysosomal enymes, lymphokines

Inflammatory cells

Differentiation of leucocytes

Inflammatory cellsMORPHOLOGY FEATURES MEDIATORS

PMNs •Initial phagocytosis of bacteria & foreign body•Acute inflammatory cell

•Primary, secondary & tertiary granules•Reactive oxygen metbolites

MONOCYTES/ MACROPHAGES

•Bacterial phagocytosis•Chronic inflammatory cell •Regulate lymphocyte response

•Acid & neutral hydrolysis•Cationic protein•Phospholipase •Prostglandinds & leukotrienes•IL-I

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

•B cells: antibody production•T cells- delayed hypersenstivity, cytotoxicity

Inflammatory cells

MORPHOLOGY FEATURES MEDIATORS

PLASMA CELL •Derived from B cells•Chronic inflammatory cells

•Antibody synthesis•Antibody secretion

EOSINOPHIL •Allergic states•Parasitic infestations•Chronic inflammatory cell

•Reactive oxygen metabolites•Lysosomal•PGE2 synthesis

BASOPHIL/ MAST CELL •Receptor for IgE molecules•Electron dense granules

•Histamine •Leukotrienes•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 µm

• 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 & Ɣ-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 macrophagesin 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. Langerhan’s 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)

Necrosis of additional tissue

Increased tissue pressure

Circumferential vascular disturbanceRelease of intracellular inflammatory agents

Local necrosis

Ischaemia

Vascular stasis

Venous collapse

Increased local tissue pressure

Localized pulpal inflammation

Release of inflammatory mediators(BK,5-HT,PGs)

Release of neuropeptides(SP & CGRP)

Total pulpitis

The vicious cycle of pulpal

inflammation

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,IMMUNOGLOBULINS-IgG,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 micro-organisms 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