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Shibu lijack

EDEMA AND CYST

FORMATIONSUBMITTED BY ;-

AKANKSHA SRIVASTAVA

INTERN

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Edema

Edema is a condition of abnormally large fluid

volume in the circulatory system or in tissues

between the body's cells (interstitial spaces).

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Description

Normally the body maintains a balance of fluid in tissues byensuring that the same of amount of water entering the body

also leaves it.

The circulatory system transports fluid within the body via itsnetwork of blood vessels.

The fluid, which contains oxygen and nutrients needed by the

cells, moves from the walls of the blood vessels into the body'stissues.

After its nutrients are used up, fluid moves back into the blood

vessels and returns to the heart.

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The lymphatic system (a network of channels in the body that

carry lymph, a colorless fluid containing white blood cells to

fight infection) also absorbs and transports this fluid.

In edema, either too much fluid moves from the blood vessels

into the tissues, or not enough fluid moves from the tissues

back into the blood vessels.

This fluid imbalance can cause mild to severe swelling in one

or more parts of the body.

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Edema formation

Increased capillary pressure the pre capillary arteriole auto

regulates capillary pressure.

Therefore, increases in capillary pressure are generally due toincreased venous pressure,

venous abstruction

eg. Venous thrombosis - expanded venous blood volume.

eg. Heart failure or kidney failure.

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Decreased plasma oncotic pressure- Hypoalbuminemia

generally

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Lymphatic obstructionuncommon, usually secondary tumor.

Sodium retention

Inflammation

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CYST: A cyst can be defined as a pathological

cavity lined by epithelium having fluid, semi-

fluid or gaseous contents but not created by

accumulation of pus.

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True cyst

Cyst with epithelial

lining.

EX: *radicular cyst

*dentigerous cyst

Pseudo cyst

Cyst without Epithelial

lining.

EX: *aneurysmal bone cyst

*traumatic bone cyst

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The pathogenesis of cysts considered to occurin three phases:

The phase of initiation

The phase of cyst formation

The phase of enlargement.

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It is generally agreed that the epithelial-linings of these cysts

are derived from the epithelial cell rests of Malassez in the

periodontal ligament.

Which come to lie in periapical granulomas associated withteeth with dead, often infected, pulps.

There is also no doubt that these cell rests may proliferate, and

when they do so, either in vivo, or in tissue culture

experiments, there are consistent morphological and

histochemical changes .

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Precisely how these epithelial cells are stimulated to proliferate

is not clear.

It would seem that some product of a dead pulp may initiate theprocess and that at the same time it evokes an inflammatory

reaction, as there is evidence that proliferating odontogenic

epithelium is associated with the presence of an acute

inflammatory cell infiltration .

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There is also some evidence that local changes in the

supporting connective tissue may be responsible for activating

the cell nests and that a decreased oxygen and increasedcarbon dioxide tension and a local reduction in pH produced

in chronic inflammation may be the critical factors.

Suggestions have also been made about the role of immunefactors in the proliferation of epithelial cell nests.

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Stern et al. (1981) showed that 74 per cent of the antibody-

producing lesional cells in periapical granulomas and cysts

synthesized IgG, 20 per cent IgA, 4 per cent IgE and 2 per

cent IgM.

The antigens involved are presumed to be derived from

bacteria.

When these antigens gain entrance to the pulp or periapical

tissues at certain concentrations, antigen-antibody complexes

may form.

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These may coactivate complement, leading to increased

vascular permeability and a leukotactic response.

Infiltrates of T lymphocytes, indicating that cellular immune

reactions are involved in their pathogenesis, were

demonstrated by Stern et al. (1982) and by Skaug et at. (1984)

in human periapical granulomas.

While the latter authors (Skaug et al., 1984a) concluded that

because of low complement component C3dreceptor activity,

B lymphocytes form only a minor component of the

mononuclear cells in these lesions.

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Proliferating epithelium has a characteristic histological appearance.

The epithelium, in section, forms arcades and rings, each encircling

a core of vascular connective tissue.

When the epithelial cells proliferate, they do so in different planes,

forming a mass rather than sheets or strands.

Cores of vascular connective tissue extend into the epithelial mass

from all directions and the resulting appearance in histological

section is one of arcades and rings of epithelial cells surrounding

these cores.

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The next phase in the pathogenesis of a radicular cyst is the process

by which a cavity comes to be lined by the proliferating odontogenic

epithelium.

Two possibilities have been generally recognized, both of which are

feasible and which may operate independently of one another.

One concept proposes that the epithelium proliferates and covers the

bare connective tissue surface of an abscess cavity or a cavity which

may occur as a result of connective tissue breakdown by proteolytic

enzyme activity (Summers, 1974).

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The demonstration of high levels of acid phosphatase activity in

the central cells of apical granulomas and in the exfoliating

epithelial cells of radicular cysts suggest that these cells are

undergoing autolysis.

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In some periapical lesions, sheets of epithelial cells with distinct

clefts are seen and in certain instances the cyst may be initiated in

this way.

Torabinejad (1983) has postulated, however, that it is not the lackof blood supply which accounts for the death of the central

epithelial cells in an apical lesion, but that the development of the

cavities in proliferating epithelium and the final destruction of

these cells are mediated by immunological reactions.

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Toller's studies provided evidence for the hypothesis that osmosis

makes a contribution to the increase in the size of cysts.

Lytic products of the epithelial and inflammatory cells in the cystcavity provide the greater numbers of smaller molecules which

raise the osmotic pressure of the cyst fluid.

Electrophoretic studies of the fluids of radicular and other non-keratinizing cysts have shown that more than half display levels of

gamma-globulin much higher than the patient's own serum.

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Toller believed that this evidence suggests that there is an

antigenic stimulus in the cyst wall and in the absence of

demonstrable infection either the occult epithelium or its

breakdown products are antigenic.

This may be the mechanism whereby cysts undergo

spontaneous regression.

Those people who have a particular tendency to develop cysts

may have an ineffective immunological surveillance and

suppression mechanism.

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Toller (1966b) also proposed the hypothesis that the contents

of cyst cavities are subject to an osmotic imbalance with the

surrounding tissues because of the absence of lymphatic

drainage.

The view that the cyst wall functions as a simple

semipermeable membrane is therefore probably an

oversimplification.

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Suzuki (1975) also demonstrated that there is an active

transport mechanism for Na+ and K+ ions across the cyst wall

and that there was a selective mechanism for the transfer of

protein.

Harris and Goldhaber (1973) postulated that intraosseous cyst

expansion is facilitated by local enzyme or hormone-induced

bone resorption and suggested that the active principle is a

prostaglandin.

It was shown that cyst walls did release prostaglandin-like

material in tissue culture.

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Epithelial proliferation continues as long as there is an

inflammatory stimulus.

When the stimulus to epithelial proliferation ceases, a situation

which often occurs in a residual cyst, the epithelium is able to

differentiate to a certain extent although keratinization is very

rare.

Further increase in the capacity of the cyst cavity at this stage

probably leads to thinning of the epithelial lining.

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Robbins basic pathology - Vinay Kumar, Stanley Leonard

Robbins

Cysts of the Oral and Maxillofacial Regions - MervynShear, Paul Speight, Paul M. Speight.

Shafer'S Textbook Of Oral Pathology (6Th Edition)-

Rajesndran- 2009

http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Vinay+Kumar%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Stanley+Leonard+Robbins%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Stanley+Leonard+Robbins%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Mervyn+Shear%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Mervyn+Shear%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Paul+Speight%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Paul+M.+Speight%22http://books.google.co.in/books?id=Spk0V6TrCggC&printsec=frontcover&dq=shafer&hl=en&sa=X&ei=NC9zT4HWNYLsrAf207XYDQ&sqi=2&ved=0CEsQ6AEwBAhttp://books.google.co.in/books?id=Spk0V6TrCggC&printsec=frontcover&dq=shafer&hl=en&sa=X&ei=NC9zT4HWNYLsrAf207XYDQ&sqi=2&ved=0CEsQ6AEwBAhttp://www.google.co.in/search?hl=en&sa=X&biw=1280&bih=685&tbm=bks&tbm=bks&q=inauthor:%22Rajesndran%22&ei=uS9zT6TjNIrPrQejspzSDQ&ved=0CDEQ9Aghttp://www.google.co.in/search?hl=en&sa=X&biw=1280&bih=685&tbm=bks&tbm=bks&q=inauthor:%22Rajesndran%22&ei=uS9zT6TjNIrPrQejspzSDQ&ved=0CDEQ9Aghttp://books.google.co.in/books?id=Spk0V6TrCggC&printsec=frontcover&dq=shafer&hl=en&sa=X&ei=NC9zT4HWNYLsrAf207XYDQ&sqi=2&ved=0CEsQ6AEwBAhttp://books.google.co.in/books?id=Spk0V6TrCggC&printsec=frontcover&dq=shafer&hl=en&sa=X&ei=NC9zT4HWNYLsrAf207XYDQ&sqi=2&ved=0CEsQ6AEwBAhttp://books.google.co.in/books?id=Spk0V6TrCggC&printsec=frontcover&dq=shafer&hl=en&sa=X&ei=NC9zT4HWNYLsrAf207XYDQ&sqi=2&ved=0CEsQ6AEwBAhttp://books.google.co.in/books?id=Spk0V6TrCggC&printsec=frontcover&dq=shafer&hl=en&sa=X&ei=NC9zT4HWNYLsrAf207XYDQ&sqi=2&ved=0CEsQ6AEwBAhttp://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Paul+M.+Speight%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Paul+Speight%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Mervyn+Shear%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Mervyn+Shear%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Mervyn+Shear%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Stanley+Leonard+Robbins%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Stanley+Leonard+Robbins%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Vinay+Kumar%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Vinay+Kumar%22http://www.google.co.in/search?tbo=p&tbm=bks&q=inauthor:%22Vinay+Kumar%22