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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
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