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Cysts of jaws pathogenesis
1. Radicular cyst
• Most common cystic lesion
• Men
• Max. anterior region (reasons)
• Painless unless infected
• Nonvital tooth
• Sinus
2. Pathogenesis
• From epithelial cell rests of mallasez
3 PHASES…,
• Phase of intiation
• Phase of cyst formation
• Growth and enlargement of the the radicular
cyst
3. Phase of intiation
o Inflammation (necrotic pulp, bacterial debris)
o Bacterial endotoxins* (Aa, p. gingivalis, e. coli)
o Immunoglobulins (IgG) , Langerhan’s cells
o T – Lymphocytes.
o Inflammatory Cytokines(IL- 1, TNF)
o Increase in size decreased O2 and increased
CO2 tension decreased pH proliferation of
cell rests of Mallasez.
4. Phase of cyst formation
o Release of proteolytic enzymes
o Degeneration and death of cells in the center
o Connective tissue breakdown along with
proliferation of surrounding epithelium may
result in formation of several microcysts.
o Several microcysts increase in size coalase to
form a single established cyst.
5.
6.
7.
8. Phase of growth and enlargement
• Lytic products of the epithelial and inflammatory cells
• raise the osmotic pressure of the cyst fluid.
• Cyst walls have property of semipermiable membrane
• osmosis across the cyst wall
• Increase in size of the cyst
9.
10. • How to differentiate between a periapical
granuloma and a cyst radiologically??
11. • Past data certainly indicate that one cannot rely on
the size of the lesion to establish a diagnosis except
where the radiographic lesion is 2cm in diameter or
larger.
• Because histologically, 1/3rd of lesions measuring
10-14 mm are proved to be granulomas and 1/3rd of
the lesions less than 5mm are proved to be as
cysts!!!
• It means there are smaller cysts and evn larger
granulomas.
• Recent studies state that it may be feasible to
differentiate between radicular cysts and periapical
granulomas on the basis of radiographic density.
(***further studies are required***)
12. Dentigerous cyst
• Dentigerous cyst develops around an
unerupted tooth by accumulation of fluid
between the reduced enamel epithelium and
the enamel, or between layers of reduced
enamel epithelium
• Now the question is how does this happen???
13.
14. • pressure exerted by a potentially erupting
tooth on an impacted follicle
• obstructs the venous outflow
• induces rapid transudation of serum across the
capillary walls.
• The increased hydrostatic pressure of this
pooling fluid separates the follicle from the
crown, with or without reduced enamel
epithelium.
15. • With time capillary permeability is altered so as to
permit the passage of greater quantities of protein
above the low concentration of the pure
transudate.
• Other factors which increase the osmolality of
cystic fluid is Glycosaminoglycons (predominantly
hyaluronic acid but also appreciable amounts of
heparin and chondroitin-4-sulphate)
16. • Why the apices of adjacent teeth are more
commonly resorbed in dentigerous cyst when
compared to other cysts?
17. • Reason is PGE2 , a prostagladin which had a
role in resorption of cementum and dentin is
released in higher amounts from dentigerous
cyst.
• This PGE2 along with PGE3 results in in
resorption of bone, and consequently the
enlargement of dentigerous as well as of other
cysts.
18. • Other bone resortion factors associated with
dentigerous cyst are cytokeratins, epidermal
growth factors, BMP-4 , epithelial membrane
antigen, Carcino embryonic antigen.
• In various studies all these are found to be
associated with dentigerous cyst.
19. • How will you differentiate between a dilated
follicle and dentigerous cyst??
20. • Some unerupted teeth have a slightly dilated
follicle in the pre-eruptive phase. This does not
signify a cyst, nor even necessarily a potential
cyst unless the pericoronal width is at least 3–
4mm.
• After several studies it is concluded that it can
be difficult to distinguish between a small
dentigerous cyst and a large dental follicle
despite the availability of both radiographical
and histological information.
21. • Is there a chance of development of a
dentigerous cyst from radicular cyst of a
deciduous teeth??
22. • After several studies it was concluded that
inflammatory change at the apex of a
deciduous tooth may be responsible for
initiating a dentigerous cyst of the permanent
successor.
24. • No evidence to support such a contention.
• Indeed, the fact that dentigerous cysts are
rarer in South African blacks, compared with
whites, whereas ameloblastomas are very
much more common in blacks.
25. • Much of the confusion has probably arisen for two
important reasons.
• First, an ameloblastoma, like an OKC, may involve
an unerupted tooth, particularly a third molar at
the angle of the mandible, and this may be
incorrectly interpreted as a dentigerous cyst on
radiographs
• When subsequently the lesion is removed and
diagnosed histologically as an ameloblastoma, the
erroneous conclusion may be reached that the
ameloblastoma developed from the dentigerous
cyst.
26. • Second possible reason for believing that many
ameloblastomas develop from dentigerous cysts is
that biopsies of ameloblastomas may be taken of
an expanded locule lined apparently by a thin
layer of epithelium. If the surgeon’s provisional
diagnosis is dentigerous cyst because of the
radiological picture, the pathologist may well
regard such histological features as consistent with
this diagnosis. When the tumour is removed
entirely and a diagnosis of ameloblastoma is
made, once again this may be misinterpreted as
having developed from a dentigerous cyst.
33. • A cystic lesion in which the epithelial lining shows
a well-defined basal layer of columnar cells, an
overlying layer that is often many cells thick and
that may resemble stellate reticulum, and masses
of “ghost” epithelial cell that may be in in the
epithelial lining or in the fibrous capsule The
“ghost” epithelial cells may become calcified.
Dysplastic dentine may be laid down adjacent to
the basal layer of the epithelium and in some
instances the cyst is associated with an area of
more extensive dental hard tissue formation
resembling that of a complex or compound
odontoma.
34. • Formation of COC is also similar to that of other
cysts but the major difference is CALCIFICATIONS
AND GHOST CELLS.
So, here the things to be discussed are…
• How these calcifications occur??
• What are these ghost cells??
• Are they associated with only COC??
35. • Intra-osseous lesions as generally being unilocular
radiolucencies with well-circumscribed borders
and variable amounts of radiopaque material
being present.
• epithelial lining of a calcifying odontogenic cyst
appears to have the ability to induce the
formation of dental tissues in the adjacent
connective tissue wall;
36. • Ghost cells that are so characteristic a feature of
the calcifying odontogenic cyst also occur in
other odontogenic cysts, the craniopharyngioma
and the calcifying epithelioma of Malherbe, as
well as in the other odontogenic tumours
• So, the mere presence of ghost cells in a lesion
does not justify the diagnosis of calcifying
odontogenic cyst.
37. • The ghost cells are enlarged, ballooned, ovoid
or elongated elliptoid epithelial cells. They are
eosinophilic and although the cell outlines are
usually well-defined, they may sometimes be
blurred so that groups of them appear fused. A
few ghost cells may contain nuclear remnants
but these are in various stages of degeneration
and in the majority all traces of chromatin have
disappeared leaving only a faint outline of the
original nucleus. The ghost cells represent an
abnormal type of keratinisation and have an
affinity for calcification.
38. NASOPALATINE DUCT CYST
• The epithelial-lined cysts of non-odontogenic
origin had been thought to be derived from
embryonic epithelial residues in the
nasopalatine canal and, in the opinion of
many workers, from epithelium included in
lines of fusion of embryonic facial processes.
(CONTROVERSIAL)
39. Nasolabial cyst
• The only cyst of the oral regions other than
the aneurysmal bone cyst to show a female
preponderance.
40. • nasolabial cyst was considered as the soft
tissue equivalent of the globulomaxillary cyst.
It was therefore suggested that it arose from
epithelium enclaved at the site of fusion of
the globular, lateral nasal and maxillary
processes. (CONTROVERSIAL).
41. • According another hypothesis, it is Developed
from the lower anterior part of the
nasolacrimal duct.
• The mature nasolacrimal duct is lined by
pseudostratified columnar epithelium and this
is the type of epithelium usually found lining
nasolabial cysts.
44. • Previously, it had been thought that these
cysts developed from epithelium entrapped in
the process of fusion of embryonic processes.
• It is now believed that they represent
posterior extension of an incisive canal cyst in
the case of median palatine cyst; anterior
extension in the case of median alveolar cyst;
and a range of other odontogenic cysts,
frequently an odontogenic keratocyst, in the
case of the globulomaxillary cysts.
• So, they were excluded from the 1992 WHO
Classification of epithelial jaw cysts
45. Keratocystic odontogenic tumour
• There has been a great deal of interest in the
odontogenic keratocyst (OKC) since it became
apparent that it may grow to a large size
before it manifests clinically and that, unlike
other jaw cysts, it has a particular tendency to
recur following surgical treatment.
46. • Intiates by proliferation of cells of dental
lamina
• Later enlargement occurs
• This enlargement depends on various factors
• And the factors are…..
47. Rate of growth
• As they tended to extend along the cancellous
component of the mandible without producing
noteworthy expansion of the cortical plates,
they frequently reached a large size before
they were diagnosed.
• Few say it has fast rate of growth, and few say
it has normal rate of growth
48. Role of osmolality in growth of the
cysts
• mean osmolality of the OKCs (approx 296 mOsm)
• mean serum osmolality (282 mOsm)
• It is strongly believed that the raised osmolalities
have an important role in the expansive growth in
the size of the OKC as well as other jaw cysts.
49. Role of inflammatory exudate in
growth of the cysts
• Inflammatory exudate has a negligible role in
OKC enlargement.
• Its cavity fluid contains low quantities of
soluble protein, composed predominantly of
albumin and only relatively small quantities of
immunoglobulins
50. Role of glycosaminoglycans in growth
of the cysts
• Hyaluronic acid showed the highest frequency
and abundance in all three cyst types.
• Appreciable amounts of chondroitin-4-
sulphate were also observed, particularly in
the radicular cysts.
• Heparin sulphate showed a higher frequency
and abundance in the OKC than the other
cysts.
51. • Mast cells were widespread in the connective
tissue of all cyst types, particularly adjacent to
the epithelium, and were probably the source of
the heparin.
• Degranulating mast cells released heparin and
hydrolytic enzymes and the latter facilitated the
breakdown of the glycosaminoglycans and
proteoglycans.
52. Role of collagenolytic activity in
growth of the cysts
• No similar activity was demonstrable in
dentigerous cysts and it was tentatively
proposed that enzymatic mechanisms may be
important in the growth of OKCs.
• Human OKC collagenase degraded types I and
II collagens at almost equal rates, but during
the same time period no significant
degradation of type III collagen occurred, a
feature that also characterised human
polymorphonuclear (PMN) type collagenase.
(‘PMN-like’ characteristics)
53. Role of Interleukins,
tumour necrosis factor,
matrix metalloproteins,
tenascin, fibronectin and collagen IV,
myofibroblasts,
parathyroid hormone related protein
54. • IL-1 , TNF OSTEOCLAST ACTIVATING FACTORS
are found to be associated with osteolysis of
OKC and other cysts
• IL-1 ἀ is the principal osteolytic cytokine
produced by OKCs leading to bone resorption.
• MMP-1 should be regarded as a significant
mediator of tissue destruction in these cysts.
• MMP-2, demonstrated strongly the proteolytic
activity of cyst tissue and its active role in the
expansion of the cysts
55. • authors investigated the immunocytochemical
expression of PTHrP in odontogenic cysts
because of evidence that OKCs have less bone
resorbing capacity than the dentigerous and
radicular cysts.
• It is a protein as the putative cause of the
humoral hypercalcaemia of malignancy, which
has potent parathormone-like activity and is a
local factor which regulates cell growth and
differentiation.
• OKC linings expressed significantly higher levels
than those of the dentigerous (P <0.003) and
the radicular (P <0.003) cysts.
56. • What are the Possible reasons for recurrences
of OKC??
57. • The first of these is related to their tendency to
multiplicity in some patients, including the
occurrence of satellite cysts which may be
retained during an enucleation procedure.
• Second, OKC linings are very thin and fragile,
particularly when the cysts are large, and are
therefore more difficult to enucleate than cysts
with thick walls.
• epithelial linings of OKCs had intrinsic growth
potential
58. • OKCs may also arise from proliferations of the
basal cells of the oral mucosa, often referred
to as basal cell hamartias, particularly in the
third molar region and ascending ramus of the
mandible.
59. • What is the reason for scalloping , multilocular
and loculated outlines in OKC ?????
60. • Multicentric pattern of cyst growth brought
about by the proliferation of local groups of
epithelial cells against the semi-solid cyst
contents.
• More than one epicenters of growth and with
unequal growth activity
• Distance between two adjacent epicenters
determines the extent of locularity.
Notas del editor
(this is the reason for arcading pattern in periapical granuloma and cyst histologically)
It is also thought that cleft formed in between the proliferating epithelial cysts may result in intiation of a radicular cyst
This small cyst is lined by proliferating epithelium
Quiescent epithelium lining a mature, long-standing
radicular cyst
Metaplasia of cystic lining resulted in formation of mucous cells and cilited columnar cells
In approximately 10% of radicular cysts, hyaline bodies, first described by Dewey often referred to as Rushton’s hyaline bodies, are found in the epithelial linings Only very rarely are they present in the fibrous capsule. The bodies measure up to about 0.1mm and are linear, straight or curved or of hairpin shape and sometimes they are concentrically laminated. They are brittle and frequently fracture. Circular or polycyclic bodies are also seen with a clear outer layer surrounding a central granular body.
secondary enamel cuticle or probably a form of keratin or bodies of hematogenous origin formed from thrombi of venules hat got strangulated by epithelial cuffs
Lytic products of the epithelial and inflammatory cells in the cyst cavity provided the greater numbers of smaller molecules which raised the osmotic pressure of the cyst fluid.
What we see here are cholesterol clefts…, earlier in these plases lies hemosiderin and cholesterol.., the main source of cholesterol was from disintegrating red blood cells in a form that readily crystallises in the tissues. Other possible sourse is plasma lipids as in the case of atherosclerosis.., Once the cholesterol crystals have been deposited in the fibrous capsules of the cysts, they behave as foreign bodies and excite a foreign body, giant cell reaction (Fig. 11.14). In histological sections, the cholesterol crystals are dissolved out and clefts are seen surrounded by dense aggregations of multinucleate giant cells. The cholesterol masses are extruded from the fibrous wall by the foreign body reaction. Invariably, the path of least resistance is into the cyst cavity as the external surface of the cyst may consist of dense fibrous tissue, bone and mucosa. When the reaction reaches the epithelial lining, this ulcerates. The granulation tissue containing the cholesterol protrudes into the cyst cavity and appears macroscopically and microscopically as a ‘mural nodule’
pressure exerted by a potentially erupting tooth on an impacted follicle obstructs the venous outflow and thereby induces rapid transudation of serum across the capillary walls. The increased hydrostatic pressure of this pooling fluid separates the follicle from the crown, with or without reduced enamel epithelium.
While ameloblastomas, being of odontogenic
epithelial origin, may theoretically arise from
dentigerous cyst lining as well as any other odontogenic
epithelium, the belief that it commonly arises in this situation
and that the dentigerous cyst should therefore be
regarded as pre-ameloblastomatous, should be viewed
with caution.
Diagram illustrating the possible
pathogenesis of the lateral periodontal cyst. (a)
There is expansion of the follicle on the lateral
surface of the crown of the unerupted tooth.
At this stage a radiograph would show what
appeared to be a lateral dentigerous cyst. (b–d)
The tooth erupts leaving the expanded follicle
behind
Botryoid odontogenic cyst developing from a lateral
periodontal cyst. There are numerous daughter microcysts, many
of which also show epithelial plaques. These plaques may be
‘pinched off’ to form granddaughter cysts.
Pinched off’ plaques forming further microcysts
Diagram illustrating the possible histogenesis of the
developmental lateral periodontal cyst (a) and the gingival cyst
of adults (b). The lateral periodontal cyst is formed from the
reduced enamel epithelium by dilatation of the follicle before
eruption of the tooth, whereas the gingival cyst of adults is
derived from reduced enamel epithelium after eruption of the
tooth.
suggested that the majority of OKCs
would take about 6years to recur to a clinically significant
size of more than 1 cm diameter but with a wide time
range, varying from 1 to 25 years.
They have referred to the frequent observation
of perforation of the overlying bone and firm adhesion of
the cysts to the overlying mucosa and recommended that
when the cysts were surgically removed, the overlying
mucosa should be excised with them in an attempt to
prevent possible recurrence or the formation of new cysts
from residual basal cell proliferations.