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EDEMA AND EDEMA AND CYST CYST

FORMATIONFORMATIONSUBMITTED BY ;- AKANKSHA SRIVASTAVA

INTERN

Edema

Edema is a condition of abnormally large fluid volume in the circulatory system or in tissues between the body's cells (interstitial spaces).

Description Normally the body maintains a balance of fluid in tissues by

ensuring that the same of amount of water entering the body also leaves it.

The circulatory system transports fluid within the body via its network 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's tissues.

After its nutrients are used up, fluid moves back into the blood vessels and returns to the heart.

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.

Edema formation

Increased capillary pressure – the pre capillary arteriole auto regulates capillary pressure.

Therefore, increases in capillary pressure are generally due to increased venous pressure,

venous abstruction

eg. Venous thrombosis - expanded venous blood volume.

eg. Heart failure or kidney failure.

Decreased plasma oncotic pressure- Hypoalbuminemia generally <2g/dl (normal 4-5 g/dl) can be seen with nephrotic syndrome and liver failure.

Increased capillary permeability – augments transudation of protein into interstitium , therefore decreases oncotic pressure gradient eg. Burns, angioedema.

Lymphatic obstruction – uncommon, usually secondary tumor.

Sodium retention

Inflammation

Formation of Formation of cyst cyst

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.

Introduction

CYST

True cyst

Cyst with epithelial lining. EX: *radicular cyst *dentigerous cyst

Pseudo cyst

Cyst without Epithelial lining.

EX: *aneurysmal bone cyst *traumatic bone cyst

FORMATION OF CYST

The pathogenesis of cysts considered to occur in three phases:

The phase of initiation

The phase of cyst formation

The phase of enlargement.

The phase of initiation

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 with teeth 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 .

Precisely how these epithelial cells are stimulated to proliferate is not clear.

It would seem that some product of a dead pulp may initiate the

process 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 .

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 increased carbon 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 immune factors in the proliferation of epithelial cell nests.

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.

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 C3d receptor activity, B lymphocytes form only a minor component of the mononuclear cells in these lesions.

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.

The phase of cyst formation

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).

The other, and perhaps more widely supported theory, postulates that a cyst cavity forms within a proliferating epithelial mass in an apical granuloma by degeneration and death of cells in the centre.

There is histological evidence for the latter hypothesis. The proliferating epithelial masses show considerable intercellular oedema.

These intercellular accumulations of fluid coalesce to form microcysts containing epithelial and inflammatory cells .

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.

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 lack of 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.

The phase of enlargement

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 cyst cavity 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.

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.

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.

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.

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.

REFRENCES

Robbins basic pathology - Vinay Kumar, Stanley Leonard Robbins

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

Shafer'S Textbook Of Oral Pathology (6Th Edition) -Rajesndran - 2009