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RATIONALE OF ENDODONTIC TREATMENT INTRODUCTION INFLAMMATION -

Definition

-

Causes

-

Signs and Symptoms

-

Cells of inflammation

-

Inflammatory process

-

Tissue change

-

Periradicular manifestation

-

Repair

ENDODONTIC IMPLICATION

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INTRODUCTION: The term “Rationale” can be defined as the fundamental reason or the rational basis for a procedure. The rationale for endodontic therapy is based on the belief that a natural tooth function more efficiently and comfortably than a bridge, partial denture or an implant tooth. Endodontic

therapy

allows

the

removal

of

vital

or

necrotic pulp from the canal system of an infected tooth and replaced by an inert filling material. This is mainly done to prevent extension of the disease from the pulp into the periapical tissues. INFLAMMATION: Definition: Can be defined as a local physiologic response of a living tissue to injury. The main objective of inflammation is to destroy the irritant causing tissue changes and bring back the tissue to a normal form and function. Mediators of inflammation: The agents that cause the changes in inflammation, the alterations in the blood vessels, the escape of proteins and cells into the tissues, and the change in the tissue – are called the mediators of inflammation. The initiated, transient vasoconstriction in due to the direct stimulation of the blood vessels and the flare is caused by an/ or on reflex. “Nerves process.”

are

not

Inflammation

necessary develops

for

the

normally

inflammatory in

derivated

tissue, except that the flow is absent. Nerves may play some part in modifying the severity of the vascular change, but in most circumstances their effect is slight.

2


Agents causing inflammation: a. Physical agents: Heat, cold, mechanical trauma as in sports

injuries,

bruxism,

cavity

preparation,

accidental

rapid

tooth

exposure movement

during during

orthodontic treatment. b. Chemical agents: ZnPO 4 , Silicate, acid etching agents etc. c. Infection agents: Bacterial, Virus, Parasites. d. Immunological agents: Cell mediated reaction antigen – antibody, reaction. Factors modifying the inflammatory respond 1)

Host resistance

2)

Intensity

3)

Duration

4)

Virulence

of

irritant

/

microorganism

(pathogenicity of stimulus). Based on these premises we can generalize that mild or moderate noxious stimuli to the pulp may produce sclerosis of

dentinal

tubules,

formation

of

reparative

dentine,

or

reversible inflammation. Irreversible injury

can

inflammatory

lead

to

necrosis

changes of

caused

pulp

and

by

severe

subsequent

pathologic changes in periradicular tissues. The inflammatory process allows: 1. The

arrival

of

phagocytic

cells

to

digest

bacteria

or

cellular debris. 2. Antibodies

to

recognize

attack

and

destroy

foreign

material. 3. Edema or fluid to distribute and neutralize the irritant. 4. Fibrin formation to limit the spread of inflammation.

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Symptoms of inflammation: According to Roman hunter Celcus in 1 s t century A.D. typical signs of inflammation can be witnessed. 1. Dolar (Pain): Caused by the action of cytotoxic agents released from humoral, cellular and microbial elements of the nerve endings. 2. Tumor

(Swelling):

Produced

by

infiltration

of

macromoleculars and fluids into the affected tissues. 3. Rubor

+

Color

(Redness

+

Heat):

Produced

by

vasodilatation of the vessels and the rushing of blood to the affected tissues. 4. Loss of function: was later added by Verchow resulting of from changes in the affected tissues. As in any other inflamed organ of the body these symptoms also occur in inflamed pulp but only pain and loss of function can be clinically appreciated because of the encasement of pulp with in dentin does not permit swelling. But in case of inflammation including the periapical tissues all

the

symptoms

of

inflammation

may

be

clinically

recognized. Cells of inflammation: Glanulocytes

Agranulocytes

- Neutrophils

- Lymphocytes

- Eosinophils

- monocytes

- Basophils The

main

cells

of

acute

inflammation

are

poly

morphonuclear neutrophil (PMN’s).

4


Chronic

inflammation:

lymphocytes,

plasma

cells,

monocytes and macrophages. Poly morphonuclear neutrophils (PMN’s) (Neutrophils or Polymorphs). 1. Their cells constitute 40-75% of Leucocytes. 2. Seen in acute inflammation. 3. They contain a. Nucleus having 2-4 lobes, which is connected. b. Cytoplasm

containing

characteristic

violet

pink

granules. These granules are said to contain enzymes i.

Lysosomes

ii.

Alkaline phosphatase

iii. Collagenase iv.

Lactoferrin

1. These cells get attached to the area of inflammation by chemotactic

factors

produced

by

bacteria

or

the

complement system. 2. They then allow the binding of opsonised bacteria onto this surface. 3. In the binding sites the bacteria are encapsulated into the neutrophils where lysosomal enzymes are released that kill the bacteria. 4. These

PMNs

have

a

narrow

range

of

life.

They

are

destroyed in the inflammatory site when the pH of the tissues falls to 6.5.

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5. This change in pH is brought about due to the release and production of lactic acid by the neutrophil during phagocytosis. 6. Destruction of the PMN’s also cause the release of 2 proteolytic enzymes. a. Pepsin b. Cathepsin These enzymes result in tissue lysis. 1. The PMN’s with the products of cellular lysis and debris are principal constituents of pairs. Eosinophils: 1. They are fewer in number, constitute, 1-6% of leukocytes. 2. They consist of; a. Nucleus usually has 2 lobes. b. Cytoplasm made up of cause deep red staining granules. 3. They are most predominant in allergic reactions and parasitic infection. 4.

During

the

immune

response,

they

are

involved

in

phagocytosis of Ag-Ab complexes and in detoxicate on of histamine. Basophils: 1. These

cells

are

least

in

number

contain

1%

of

all

can

be

incubating leukocytes. 2. They

resembles

distinguished

by

all

other

their

leukocytes

coarse

but

intensity

basophilic

granules which usually fill the cytoplasm.

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3. These granules contain Heparin, Histamine and Hydroxy tryptamine and when these granules are stimulated by tissue injury or antigen they degranulate and release these substances, which can initiate an inflammatory or a allergic response. 4. Basophils and masts cells are considered similar cells except that Basophils are found in hemopoetic system and mast cells in tissues. Functions of both these cells are same. Macrophages: 1. These

cells

Immature

are

derived

monocytes

from in

circulating

extravascular

monocytes. areas

of

such

as

inflammation differentiate into macrophages. a.

Macrophages are phagocyte cells that ingest - Cellular debris - Microorganisms - Particulate matter

b. They

release

lysosomal

mediation

enzymes,

of

inflammation

complement

proteins

and

prostaglandins. c. They enhance the immunological reaction by ingesting processing and degrading the antigen before presenting it to the lymphocytes. d. Then

capacity

to remove debris

from area facilitates

repair. e. Macrophages are mononucleated cells that, in periods of great

activity,

may

fuse

into

other

macrophages

to

produce a multinucleated giant cell.

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They release enzymes like 1. Acid hydrolases. 2. Neutral proteases, these enzymes result in digestion of dead cells. 3. Collagenase. 4. Elastase. Lymphocyte: 1. These cells appear in the chronic stage of inflammation. They are intimately related to the immunological system of the organism. 2. It is seen that immune system also fights infection along with the inflammatory process. 3. If the normal inflammatory process fails to sum up with the infection then the body mounts up a more massive highly efficient response that is capable of memory as well as specificity – viz., the immune system. The immune system is comprised of two basic. 1) B cells 2) T cells Both derived from the haemopoitic system. These cells have

a

large

spherical

or

slightly

indented

nucleus

surrounded by a thin band of cytoplasm containing small granules. The stem cells are carried by the blood to the thymus where they differentiate as T - Cells 1. In thymus they become 1.

B - Cells Become immuno

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immuno comp. T cells. 2. Most common cells of lymphocytes 3. Responsible for cell mediated immunity + immuno surveillance of the human organisms 4. Circulate through the lymphoid tissues and other organs of body except thymus. 5. Found in para cortical area of lymph nodes. 6. When stimulated by foreign body they form sensitized T. lymphocytes

7. Types a) Memory T-cells – Speed up immunological reaction when in contact with same antigen. b) Helper or suppressor cells– which stimulate or suppress the development of effects T or B cells. c) Effector T cells – Produce cell mediated immune reaction such as delayed hypersensitivity

competent in bone manner 2. Lesser in number than T cells. 3. Responsible for humoral immunity.

4.

5. Found in cortical areas of lymph nodes. 6. When stimulated by foreign body they become large cells called plasma blasts. Plasma blasts divide into c. Plasma cells d. Memory B Cells 7. Types a) Plasma cells – Large oral round cells with chromatic nucleus, which contains chromatic network in cartwheel form. These cells produce immunologlobulin or antibodies.

b) Memory B cells – speed up the immunologic reaction in subsequent encounters with same antigen. 8) Cells release chemical 8) mediations known as lymphokines 9) Lymphokinesmay 9) Immunoglobulin or activate antibodies of which have

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a) Macrophages five classes IgM, IgG, IgA, IqD & IgE. b) PMNS c) Non-sensitized T cells or d) Produce interferron which inhibits viral replication Antibodies in humoral immunity IgM: In the first antibody to be produced when host is stimulated by an antigen. Plasma cells then produce IgG. IgG + Igm: are the circulatory antibodies and one the most important of the serum antibodies. IgG + IgM base the capacity to bind to the antigen on specific receptor sites. This process is termed as Opsonization and the antibodies are called opsonins. IgA: Is found in saliva, tears etc. IgE: In conjunction with eosinophil serves a function of protection against parasitic infection. IgD: Function is not yet known but is considered to be a surface on B-lymphocytes hence triggering antigen related lymphocytes differentiation. These antibodies combine with specific antigen to form a

complex

complement

that

activates

system

then

the

compliment

release

chromatic

system.

The

factors

that

attract phagocytic cells to the area that eugenol the antigen and destroy it. Inflammatory Process Acute inflammation: This process can be studied as a. Vascular changes b. Escape of cells from blood vessels into tissues c. Tissue changes

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Vascular Changes: In any kind of injury 2 types of vascular changes can be appreciated a. Vasodilatation. b. Increase in vascular permeability Immediate response to injury results in transient vaso constriction of blood vessels, which lasts for few seconds. This is followed by vasodilatation of blood vessels that persists for day to weeks that is as long as the inflammation persists. This vasodilatation of arterioles is caused by the relaxation of anterior and capillary sphincters. As a result of vasodilatation there is increased rate of blood flow, which also

results

in

opening

of

dormant

capillary

beds

that

increases the blood supply to the affected area. This causes rise in intra vascular pressure leading to redness and heat. Simultaneously

because

of

release

of

proteolytic

enzymes from injured cells, bacterial toxins and traumatic mechanical forces, histamine is triggered off from the mast cells. This histamine contracts the endothelial cells and increases the intracellular gaps between them. These gaps along with the

intra vascular pressure results in some

plasma fluid to leave the vessels. This fluid is less in protein and is termed as inflammatory transudate. This transudate is soon over shadowed by the blood plasma

which

contains

rich

plasma

proteins

such

as

albumin, fibrinogen, immunoglobulin, which is called as inflammatory exudates. 1.

This

blood

mediation

plasma and

helps

cells

of

in

bringing

inflammation

the to

chemical start

the

inflammatory reaction. 2.

It also dilutes bacterial toxins.

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3.

It helps to form fibrin to contain the inflammatory reaction.

This

exudate

accumulates

in

the

tissue

producing edema. As the increased blood flow through the vessels fills up the capillary beds, the volume of capillary bed increases so there is slowing down of blood flow. This alteration in the caliber of blood flow results in structural changes in the micro vasculature i.e., 1. The RBCs come in the center 2. Leukocytes move towards the vessel wall. This process is called margination of leukocytes. After margination the leukocytes adhere to the vessel wall, which is termed as pavementation. After the procedure the next step is Emigration of Leukocytes. At

the

site

of

inflammation

these

leukocytes

are

attracted by -

Compliment system

-

Prostaglandins

-

Kallikrein

Which acts a chemotactic agent. This is called as ‘chemotoxis’ where the leukocytes migrate through the vessel wall by amoeboid movements. The

PMN’s

migrate

1st

followed

by

monocytes

and

lymphocytes. Simultaneously ‘Heggman factor’ or factor XII is also released into the tissue in the inflammatory exudates. This factor is activated by collagen; damaged blood vessels; Ag-Ab complexes. Reacts with PreKallikrien – Kinin. Kinin produced 1) Helps in dilatation of blood vessels,

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2) permeability of blood vessels. The Heggman factor also activates the fibrinolytic and blood co-aggulating systems. Fibrinogen XII---- Fibrin ---– confines the inflammatory reaction to a limited area. Plasminogen XII----- plasmin --- activates the complement system -

--- digests fibrin to remove blood clots.

-

---Activates kinin system.

This

complement

system

in

turn

releases

the

chemotactic factors, which aid in chemotoxis. The vascular response continues with the aggregating of RBC in the vessel causing resistance of blood flow. This

resistance

along

with

the

increase

in

blood

viscosity produced by the loss of plasma causes metabolic changes such as 1. Decrease in oxygen concentration. 2. Increase in carbon dioxide. 3. Low pH. Relating these changes to pulpal tissues as elsewhere in the body are detrimental as they prevent the removal of waste products. The spread of inflammation is faster in pulp tissue as it is in a closed chamber, which may lead to total necrosis of the pulp.

Also the migration of monocytes and

lymphocytes at the inflammatory sites start a immunologic reaction.

The

lymphocytes

macrophages, and

plasma

lymphocytes

cells

mediators

derived of

the

by

B-

immune

response are also found at the site.

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Extra

vascular

immunoglobulins

found

are

predominantly IgG apart from IgE, IgA, IgM. The recovery of pulp can be explained by some unique vascular responses. Anterior venous anastamoses and U turn loops open in the pulpal vasculature to reduce the flow to the area of inflammation there by decrease in the vascular pressure. The increased tissue pressure plays an important role in the recovery of pulp by allowing return of macromolecules and fluids to the venules. Therefore these 2 changes return the vascular pressure and tissue pressure to normal and stimulate the repair. Phagocytosis: This

is

defined

as

process

of

engulfment

of

solid

particulate material by the cells. This is carried out by cells called as Phagocytes mainly 1. PMN’s; 2. Circulating monocytes or Macrophages. Phagocytosis takes place in 3 stages 1.

Attachment

stage:

The

serum

at

the

injury

site

contains naturally occurring opsonins. These opsonins get coated on the microorganisms. Main opsonins are: 1) IgG opsonin 2) C 3 B opsonin 2. Engulfment stage: The phagocyte gets attracted to this opsonised pseudopods

microorganism that

envelop

and

sends

out

and

encloses

cytoplasmic

the

organism

forming a vacuole. The plasma membrane enclosing the phagocytic vacuole breaks. The lysosomes fuse to the phagocytic vacuole to form a phagolysosome.

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3. Degranulation stage: Degranulation takes place releasing antibacterial substances, which kills the microorganisms. The enzyme released help in digestion and liquefying of the dead cells and damaged tissues. Tissue changes following inflammation: Can be either 1. Degenerative 2. Proliferative 1. Degenerative changes: Degenerative changes in the pulp may be i. ii. iii. iv. v.

Fibrous Resorptive Calcific Necrosis Supportive

Suppuration

occurs

due

to

release

of

proteolytic

enzymes from the PMN resulting in liquifaction of dead tissue resulting in to pus formation. Accumulation of this pus forms an abscess. Requirements for pus formation a. Necrosis of tissue cells b. Sufficient number of PMN’s and Leukocytes c. Digestion of the dead material by protolytic enzymes. 2. Proliferative changes: These are produced by irritants mild enough to act as a stimulatant. Within an area, a substance may be both irritant and a stimulant. For e.g. Ca(OH) 2 in the center of inflammatory area may act as an irritant strong enough the produce regeneration or

15


distruction where as at the periphery it may be mild enough to stimulate proliferation. When a gap is present between tissue parts, repair is made by granulation tissue. Periradicular manifestations: If the inflammatory response over whelms the pulp there is partial or total necrosis of the pulp in the root canal, this serves as a pathway to the periradicular area for the

noxious

products

of

tissues

necrosis

and

antigenic

agents. The inflammatory and immunologic reaction continue in the periradicular area as in pulp In the periradicular area the noxious products cause. Bone

resorption

and

resorbed

bone

is

replaced

by

granulation tissue. The affected tissue contains neutrophils, lymphocyte, plasma

cells,

macrophages,

mast

cells

along

with

immunoglobulins IgG, IgA, IgM, IgE and complement. Some recent reports indicate that some endodontic flare -ups are mediated by IgE reactions and that have bone resorption

is

mediated

by

lymphokine

called

ostoelastic

activating factor. These findings tells us the important role that immunology plays in the physiology, and pathology of the periradicular tissue. Endodontic Implications : Fish described the reaction of periradicular tissues to noxious products of tissue necrosis, bacterial products, and antigenic agents from the root canal and established an experimental focci of injection, which he described as 4 zones. Four zones of reaction are 1. Zone of infection

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2. Zone of contamination 3. Zone of irritation 4. Zone of stimulation Zone of infection : 1. Infection is present in the center of the lesion. 2. Micro-organisms are also present only in that area. 3. It contains pus fluid, which contains i.

Dead cells.

ii.

Destructive components released from phagocyts.

iii. Intermediate

and

end

products

of

protein

decomposition (Proteolysis). 4. Main cells are polymorphoneuclear leukocytes 5. Micro-organisms are attacked by these leukocytes. 6. The microorganisms not attacked by leukocytes are found in the Haversian canals or in the fissures of bone matrix made by bur. Zone of contamination: 1. The principal difference cells are the round cells mainly ‘lymphocytes’. 2. Macrophages are less in number. These appear later because they are less motile and survive longer than neutrophils or lymphocytes. 3. Dilution of toxic elements takes place. 4. Fish observed cellular distortion around the central zone, not from bacteria themselves but from toxins discharged from the central zone. 5. Bone

cells

die

and

undergo

Autolysis.

Therefore

the

lacunae appear empty as opposed to that of the central zone. Zone of irritation: Toxicity diminishes as distance increases from central zone.

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1. Principal cells a. Macrophages. b. Osteoclass. 2. Undifferentiated cells join to form osteoclast which resorb the contaminated bone. 3. Phagocytosis

takes

place

of

collagen

network

by

macrophages and cells. 4. The activity of osteoclasts on bone open up gap in the bone all around the center of lesion. This space gets filled with leukocytes Because in this; -Healing starts to take place -Repair. 5. Capillary proliferation. 6. Cells like plasma cells, lymphocytes, macrophages etc., starts developing more from undifferentiated cells. Zone of stimulation: Toxicity reduced to mild stimulatant 1) Cells a. Fibroblasts b. Osteoblasts This

zone

takes

care

of

periphery

i.e.

peripheral

orientation takes place. 2) Collagen fibres are laid down by fibroblast which act as a. Wall of difference around zone of irritation. b. Scaffolding on which osteoblasts lays new bone. New bone is irregular in pattern. By this experiment fish concluded that root canal is a seat of infection. The microorganisms from the root canal are

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rarely motile. However they can multiply sufficiently enough to grow out of the root canal or the metabolic products of microorganisms or toxic products of tissue necrosis may diffuse into the periradicular tissue. As the microorganisms gain entry into the periradicular area they are destroyed by the leukocytes. If the number of microorganisms is less a stalemate occurs. If it is more, chronic abcess occurs. The toxic products of microorganisms and the necrotic pulp in the root canal acts as irritants and destroy the periradicular

tissues

along

with

proteolytic

enzymes

resulting in pus formation. At the periphery of the lesion there is stimulation of fibroblasts to build the fibrous tissues and osteoblasts to limit the area with a wall of sclerotic bone. This happens because

of dilution of

toxic products,

which

acts

as a

stimulant. If in addition the epithelial cell rests of mallesez are stimulated a cyst develops. Once the root canal has been treated and the reservoir of bacteria or noxious products has been eliminated and the root canal thoroughly obturated the destroyed periapical bone undergoes repair.

REFERENCES:  Grossman – Endodontic Practice.  Robbins – Basic Pathology.

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