Odontogenic Cysts Explained

ODONTOGENIC
CYSTS
Dr. Veena Desai

Content
1. Introduction
2. Classification
3. Odontogenic cyst
4. Pathogenesis of cyst
5. Developmental cyst
6. Inflammatory cyst
7. Conclusion
8. References
2

Introduction
 A cyst is defined as an epithelium-lined pathologic cavity.
 Cysts of the maxilla, mandible, and perioral regions vary markedly
in histogenesis, incidence, behavior, and treatment.
By Killey and Key (1966):
 This entity constituted an epithelium-lined sac filled with fluid or
semi - fluid material.
Clinical Pathological Correlation. Regezi, 4th edi 3

Kramer (1974)
Defined a cyst as ‘ a pathological cavity having fluid,
semifluid or gaseous content and which is not created
by accumulation of pus’.
Most cysts, but not all ,are lined by epithelium.
Cysts of the Oral and Maxillofacial Regions ,Mervyn Shear ,Fourth edition
4

 Cysts are divided into odontogenic cysts,
nonodontogenic cysts, pseudocysts, and
neck cysts.
 Pseudocysts differ from true cysts in that
they lack an epithelial lining.
Clinical Pathological Correlation. Regezi, 4th edi5

Contemporary OMFP,2nd edi,Sapp Eversole Wyso6

Classification of cyst
Cyst of Jaws
Cyst associated with
maxillary antrum
Cyst of soft tissues of the
mouth,face ,neck and salivary
gland.
7

Cyst of Jaws
Cysts of the Oral and Maxillofacial Regions ,Mervyn Shear ,Fourth edition9

Epithelial lined cyst
Developmental Inflammatory
• Radicular
• Residual
• Paradental
• Inflammatory
collateral cyst
Odontogenic Non-odontogenic
• Dentigerous
• Eruption cyst
• OKC
• Lateral Periodontal
• Gingival cyst of adult
•Gingival cyst of newborn
•Glandular Odontogenic
•Botryoid Odontogenic
• COC
• Mid-palatal
raphe cyst of
infants
• Nasopalatine
duct cyst
• Nasolabial cyst
Cysts of the Oral and Maxillofacial Regions ,Mervyn Shear ,Fourth edition10

Non Epithelial lined
Solitary Bone Cyst
Aneurysmal Cyst
11

Cyst associated with maxillary antrum
Mucocele
Retention
cyst
Post-
operative
maxillary
Cyst
Pseudocyst
12

Cyst of soft tissues of the mouth, face ,neck and salivary
gland.
13

Contemporary OMFP,2nd edi,Sapp Eversole Wyso14

Odontogenic Cyst
Contemporary OMFP,2nd edi,Sapp Eversole Wyso 15
A cyst in which the lining of the lumen is derived from
epithelium involved in tooth development

EMBRYOLOGICAL DERIVATION OF
ODONTOGENIC CYSTS
EMBRYOLOGICAL
STRUCTURE
EPITHELIAL RESIDUE ODONTOGENIC CYST
DENTAL LAMINA EPITHELIAL COILS
( rests of SERRES)
Odontogenic
Keratocyst
ENAMEL ORGAN REDUCED ENAMEL
EPITHELIUM
DENTIGEROUS CYST
EPITHELIAL ROOT EPITHELIAL RESTS DENTAL CYST
SHEATH OF HERTWIG OF MALASSEZ
R.M.Browne;The Pathogenesis Of Odontogenic Cysts: A Review. Journal of Oral Pathology 1975;4:31-46
16

Cyst Formation
 Cyst Initiation: Results in proliferation of epithelial
lining and formation of a small cavity.
 Cyst Enlargement: It is similar for all epithelium
lined cyst with some variations.
18

Theories of cyst initiation
 Grawitz theory:
 Migration of the oral cavity mucosa into the
preformed cavity.
 Siegmund-Weber theory:
 Development via intra-epithelial cyst development.
 Euler-Meyer theory :
 Development via intra- and extra-epithelial cavity
formation.
19

Cyst Enlargement
Following Mechanism are involved in cyst enlargement :
 Increase in volume of contents
 Increase in surface area of the sac and if this is lined by
epithelium,then epithelial proliferation.
 Displacement of surrounding soft tissue.
 Resorption of surrounding bone when the cyst develops
within bone.
20

Theories of cyst enlargement
Harries classification
 Mural growth
• Peripheral cell division
• Accumulation of cellular content
 Hydrostatic enlargement
• Secretions
• Transudation or exudation
• Osmotic theory of enlargement
 Bone Resorbing Factor
21

Mural growth
Peripheral cell division Accumulation of cellular content
22

Hydrostatic enlargement
Secretions-In hydrostatic enlargement fluid accumulation
within cystic cavity will cause cystic wall expansion.Secertion:Eg.
Follicular cyst (line by goblet cell).
• By the goblet cells that line the cyst
Transudation or exudation
• From capsular capillaries in the cyst
• As the immunoglobulins found in odontogenic cyst
fluids may be derived from- local synthesis in cyst
capsule & inflammatory exudate
23

Osmotic theory of enlargement
Epithelial cell break down product
Hyperosmolar cyst fluid
(draws in fluid from surrounding tissue)
Increase Hydrostatic pressure
Cyst Enlargement
Main(1970), Harris &Toller(1975) 24
As increase in hydrostatic pressure is dependent on
type of lining , its permeability and cystic content cause
cystic enlargement.

Osmotic difference detween the serum and cystic fluid is
related to protein present within the cystic fluid.
Responsible for increase in osmotic pressure of cyst.
Result in cyst expansion.
25
Protein such as
albumin,globulin,fibro
gen and fibrin
degradation product.
Mean osmolality of
cystic fluid is 10
milliosmoles higher
than that of serum.

Bone Resorbing Factor
Inflammatory cell release Lymphokines
(Osteoclast activating factor and IL-1)
Stimulate Fibroblast
Prostaglandin (PGE2 & PGE3)
Potent bone resorbing factor
Cyst Enlargement
26

The mechanism of Pg production
• One possibility is that production takes
place in the capsule under the influence
of epithelial proliferation
[Fibroblast & PMNs – ] lysosomal
phospholipase
Breaking down of phospholipid cell
membrane produce
Arachidonic acid
Arachidonic acid
Prostaglandin
synthetase
Prostaglandin

Dentigerous Cyst
follicular/ pericoronal cyst
• An odontogenic cyst that surrounds the crown of an impacted
tooth; caused by fluid accumulation between the reduced enamel
epithelium and the enamel surface, resulting in a cyst in which the
crown is located within the lumen.
(Shafer’s text book of Oral pathology, 6th edition)
• A dentigerous cyst is one that encloses the crown of an unerupted
tooth by expansion of its follicle and is attached to its neck.
(Cysts of the Oral and Maxillofacial Regions ,Mervyn Shear ,Fourth edition)
29

Frequency :
Out of 3498 jaw cyst 599 dentigerous cyst recorded in department of
oral pathology of the University of Witwatersrand, Johannesburg.
Age :
1st decade
2nd decade
3rd decade
30

•This cyst is always associated initially with the crown of an
impacted, embedded or unerupted tooth .
•A dentigerous cyst may also be found enclosing a complex
compound odontoma or involving a supernumerary tooth.

Gender :
Male > Women (3:2)
Race :
White > Black (1.6:1)
Site :
Mandibular 3rd Molar
Maxillary Canine
Mandibular 2nd Premolar
Maxillary 3rd Molar
Also associated with supernumerary tooth 90% with
maxillary mesiodens.
Supernumerary teeth may develop dentigerous cysts (Mourshed, 1964b;
• Lustmann and Bodner, 1988).
32

Clinical Presentation:
Most dentigerous cysts are solitary
•The dentigerous cyst is potentially capable of becoming an aggressive lesion.
• Expansion of bone with subsequent facial asymmetry, extreme displacement of
teeth
• severe root resorption of adjacent teeth and pain are all possible sequelae
brought about by continued enlargement of the cyst
•. Cystic involvement of an unerupted mandibular third molar may result in a
‘hollowing-out’ of the entire ramus extending up to the coronoid process and
condyle as well as in expansion of the cortical plate due to the pressure exerted by
the lesion.
•Associated with this reaction may be displacement of the third molar to such an
extent that it sometimes comes to lie compressed against the inferior border of the
mandible.
• In the case of a cyst associated with a maxillary cuspid, expansion of the anterior
maxilla often occurs and may superficially resemble an acute sinusitis or cellulitis.

 Swelling
• PainThere is usually no pain or discomfort associated with the cyst
unless it becomes secondarily infected.
 Multiple and bilateral cysts are found in association
with syndromes -
 Cleidocranial dysplasia
 Maroteaux-Lamy Syndrome
34

Radiographic feature :
 Well defined unilocular radiolucency associated
with the crown of unerupted teeth.
 Well defined sclerotic margins.
 Ocassionally trabeculae seen.
 Root resorption of adjacent tooth.
 Tooth displacement.
35
While a normal follicular space is 3–4 mm,
a dentigerous cyst can be suspected when
the space is more than 5 mm.

Radiographic varient
• Central - the crown is enveloped symmetrically. In these instances, pressure
is applied to the crown of the tooth and may push it away from its direction of
eruption. In this way, mandibular third molars may be found at the lower
border of the mandible or in the ascending ramus and a maxillary canine may
be forced into the maxillary sinus as far as the floor of the orbit.
 Circumferential
36
Lateral-which result from dilatation of the follicle on one aspect
of the crown.
This type is commonly seen when an impacted mandibular third
molar is partially erupted so that its superior aspect is exposed.

Fig. 4.1 (a) Gross specimen of a dentigerous cyst opened in the
laboratory. The cyst encloses the crown of the tooth and is
attached to
its neck. (b) Macroscopic section of a dentigerous cyst showing
attachment of its lining to the cervical margin of the tooth, enclosing
its crown.

Pathogenesis
Reduced Enamel Epithelium:
• Inner Enamel Epihelium (cuboidal or columnar)
• Outer Enamel Epithelium
• Stellate Reticulum
(Polyhedral cells)
38

• During eruption of tooth, this reduced enamel epithelium
acquire squamoid appearance.
• In case of impacted tooth this squamoid changes become
more marked.
• The attachment of the reduced enamel epithelium to the
tooth surface become weaker as it changes to squamous
type.
• The epithelial cells assumes characteristic layer of stratified
squamous epithelium.
39

Formation of cyst
Dentigerous cyst may developed either
accumulation of fluid betweem reduced enamel
epithelium and enamel surface or within enamel
organ itself.
40

Pressure [ main’s theory 1970]
(potentially erupting tooth)
Impacted follicle
Obstruct venous outflow
Serum transudation across capillary wall
Hydrostatic pressure of the pooling fluid
Separates the follicle from the crown 41

• with time ,capillary permeability is altered so as to
permit the passage of greater quantities of protein above
the low con. of the puretransudate.
• Total soluble protein level (A/G ratio) in dentigerous cyst
fluid is equal to those in serum.
• Suggesting that the fluid arise as an exudate to those from
the vessels in capsule and very little modified by local
immunoglobulins synthesis [ IgG] in the capsule.
42

Expansion of cyst
 The fluid in cystic cavity become hypertonic as
compare with serum
 Provide driven force for cystic expansion.
 A unicentric, hydrostatic growth force allows the
lesion to expand.
43

Inflammation and growth
• Many dentigerous cysts show evidence of a degree of acute
and chronic inflammation in their walls.
• The passage of desquamated epithelial cells and
inflammatory cells into the cyst cavity must contribute to the
increase in intracystic osmotic tension and further expansion
of the cyst.
44

Glycosaminoglycans and growth
• GAGs, predominantly hyaluronic acid and also appreciable
amounts of heparin and chondroitin-4-sulphate, are present in
the fluids and walls of dentigerous cysts.
• Release of GAGs from the walls and their diffusion into the
cyst fluid increases the osmolality of the cyst fluid and hence
raising the internal hydrostatic pressure of the cyst.
45

Bone resorption and growth
IL-1 released by the cyst leads to number of osteolytic cell
reactions:
 Stimulation of osteoclasts to resorb bone,
 Stimulates connective tissue cells to produce –
• prostaglandins, which is responsible for further
osteoclast activation.
• Collagenase which is involved in the destruction
of bone matrix.
46
Bone resorbing potency of this cyst is greater than okc.
IL released by – monocyte-macrophage infilterate, the stromal fibroblasts and
the epithelial cyst lining. The prostaglandins are potent bone resorbing factor.

• The epithelium proliferation in case of dentigerous cyst
can be regarded as a manifestation of its inherent
property to cover a “raw” connective tissue surface.
• Due to low mitotic rate in epithelium, the stimulus to
growth is slight.
• As the cyst expand there will be compensatory
epithelium proliferation to cover the greater
surface of CT.
47

Potential Complications. Several relatively serious
potential complications exist stemming from the dentigerous cyst, besides simply
the possibility of recurrence following incomplete surgical removal. These include
􀁏 The development of an ameloblastoma either from the lining epithelium or
from rests of odontogenic epithelium inthe wall of the cyst.
􀁏 The development of epidermoid carcinoma from the same two sources of
epithelium.
􀁏 The development of a mucoepidermoid carcinoma, basically a malignant
salivary gland tumor, from the lining epithelium of the dentigerous cyst
which contains mucussecreting cells, or at least cells with this potential,
most commonly seen in dentigerous cysts associated with impacted
mandibular third molars.

Vicker and Gorlin criteria for ameloblastoma
 When observed together as manifestation of
impending neoplasm.
 Hyperchromatism of basal cell nuclei.
 Palisading with polarization of basal cell.
 Cytoplasmic vacuolization with intercellular spacing of the
lining epithelium.
49

 Epithelial lining :
 Non-keratinized
 2-4 cell layers of flat or cuboidal cells, some time superficial layer
of epithelial lining is low columnar and retains the morphology of the
ameloblast layer.
Rete ridges absent unless secondarily infected.
Some time mucous producing cells present in lining.
The presence of mucous and ciliated cells is thought to result from
metaplasia.
Hyaline bodies sometime seen.
Histopathology
50

Thin fibrous cyst wall derived from dental follicle :
 Young fibroblast, seperated by stroma and ground
substance.
 Nest, islands and strands of odontogenic epithelium also
seen in capsule.
51
The content of cystic lumen is usually thin watery yellow fluid
and is occasionally blood tinged.

Dentigerous cyst lined by thin, nonkeratinized
epithelium
52

Dentigerous cyst lined by ciliated stratified squamous
epithelium
53

Dentigerous cyst epithelial lining containing Rushton
bodies; an incidental finding of no significance
54

ERUPTION CYST [ true soft cyst ]
 An odontogenic cyst with the histologic feature of a dentigerous
cyst that surrounds a tooth crown that has erupted through bone
but not soft tissue and is clinically visible as a soft fluctuant mass
on the alveolar ridges.
 An eruption cyst or “ eruption hematoma” is in fact a dentigerous
cyst occuring in soft tissues.
 No radiographic changes
55

ERUPTION CYST
 An odontogenic cyst with the histologic feature of a dentigerous
cyst that surrounds a tooth crown that has erupted through bone
but not soft tissue and is clinically visible as a soft fluctuant mass
on the alveolar ridges.
 An eruption cyst or “ eruption hematoma” is in fact a dentigerous
cyst occuring in soft tissues.
56

 Occur in children and in adult ,if delayed eruption.
 Circumscribed, fluctuant, translucent swelling of the alveolar
ridge at site of erupting tooth.
 When the cyst cavity contain blood, the swelling appears purple
or deep blue, hence the term ‘eruption hematoma’.
 Enlarge to size : 1- 1.5cm.
57

Eruption cyst overlying an erupting maxillary molar.
58

Pathogenesis
 Pathogenesis is similar to that of Dentigerous cyst.
 The difference is that tooth in the case of the eruption cyst is
impeded in the soft tissue of gingiva rather than in bone.
 The presence of dense fibrous tissue in the overlying
gingiva rather than in bone.
59

 Epithelial lining :
Epithelial lining of cyst is similar to Dentigerous cyst
Superficial aspect is covered with stratified squamous epithelium of
overlying gingiva.
This is seperated from cyst by a strip of dense connective tissue of
varying thickness which usually shows a mild chronic inflammatory
cell-infilterate.
Histopathology
60

Cyst wall :
Follicular CT is more densly cellular, less collagenous and has a
basophilic hue, due to higher content of acid muco-polysaccharide in
the ground substance with odontogenic epithelial cell.
61

Part of eruption cyst showing epithelial lined cyst
cavity beneath the mucosa.
62

Odontogenic Keratocyst / Keratocystic
odontogenic tumor
Developmental cyst derived from remnants of dental lamina with a
biological behaviour similar to a benign neoplasm with a distinctive
lining of 6 to 10 cells in thickness, and that exhibits a basal cell
layer of palisaded cells and a surface of corrugated parakeratin.
63

 Have potential to behave aggresively.
 Can recure.
 Can associated with syndrome.
 OKC might be regarded as benign cystic neoplasms.
 It shows clonal loss of heterozygosity of common tumor
suppressor gene.
 Finding of clonal loss deletion mutations of genomic
DNA in these cysts supports the hypothesis that they are
neoplastic rather than development in origin.
64

Terminology used by several authors for Keratocystic
Odontogenic tumor are as follow:
Hauer 1926 Cholesteatoma
Philipsen 1956
Odontogenic
keratocyst
Shear 2003 Keratocystoma
Reichart and
Philipsen
1969 Keratinizing cystic
odontogenic tumor
Philipsen 2005
Keratocystic
odontogenic tumor
65

Frequency :
Out of 3498 jaw cyst 355 OKC recorded in department of
oral pathology of the University of Witwatersrand,
Johannesburg.
Age :
Bimodal age distribution
1st Peak - 2nd and 3rd decade
2nd Peak – 5th decade
With Syndrome : Females in younger ages
66

Gender :
Male > Women
Race :
White > Black
Site :
Mandibular > Maxilla
Without syndrome : Mandibular molar-ramus area
With syndrome : Maxillary molar area
67

 Swelling
 Pain
 Discharge
 Occasionally paraesthesia of lower lip, pathological fracture.
 Multiple OKCs – Gorlin-Goltz syndrome
(Nevoid basal cell carcinoma syndrome)
Marfan
Ehler’s Danlos syndrome
68
On aspiration there is
odorless creamy or caseous
content.

• Maxillary cyst – may involve maxillary sinus, displacement
and destruction of floor of the orbit and proptosis of the eye
ball.
• May involved the base of the skull, behaving rather like a
low grade squamous cell carcinoma .
• They may penetrated the cortical bone and involved
surrounding soft tissue:
• 1/3 maxillary cyst – buccal expansion
• Palatal expansion is very rare
• ½ mandibular cyst – buccal expansion
• 1/3 mandibular cyst – lingual expansion
69

 Unilocular radiolucency with well-defined peripheral
rim.
 Scalloping of border-Scalloping is due to unequal growth
activity take place in different parts of the cyst lining.
 Multilocular radiolucency representing central cavity
having satellite cyst.
 Sometime it may displace neurovascular bundles.
 Root resorption of adjacent tooth comparatively less as
compare to dentigerous cyst.
70

Recurrences
A recurrent OKC may develop in three different ways-
 By incomplete removal of original cyst lining.
 By the retention of daughter cysts from microcysts or
epithelial islands in the wall of original cyst.
 By development of new OKCs from epithelial off-shoots
of the basal layer of oral epithelium.
72

Pathogenesis
Two main sources of the epithelium from which the
cyst is derived:
 The dental lamina or its remnants
 Extensions of basal cells from the overlying oral
epithelium.
73

Formation of cyst
 Two theories of origin are compatible, as both dental
lamina and basal cell hamartias have common
parentage (the stomadeal ectoderm).
 Both are influenced by ectomesenchyme or residual
ectomesenchymal inductive influences.
 It seems reasonable to speculate that the mucosal basal
cells could be targeted by the same genetic influences
as dental lamina.
74

 There are frequently groups of epithelial cells
apparently derived from the dental lamina in the
capsule of OKC.
 These often form satellite cysts, suggesting that there
is a clone of epithelial remnant of the dental lamina
which are genetically abnormal and prone to
exuberent proliferation.
75

 Thus satellite cysts are formed when islands of proliferating
epithelial cells derived from small epithelial rests reach a size
where cystic breakdown occurs.
 The importance of this epithelial proliferation in the growth of
the OKC is confirmed by their multilocular and loculated
radiographic features.
76

Expansion of cyst
• Rate of growth:
 Rate of growth of OKC varies from 2 to 14 mm a year
(average-7mm).
 Growth is more unremitting.
 The mitotic value of OKC lining ranged from 0 to 19 (mean-
8.0)
 Nuclear morphometric variables of the epithelium of OKC
showed that the numbers of cells in the basal layer was higher
and its nuclei were more ovoid and more variable in size than
other cysts
77

Role of osmolality in growth of the cysts
 Total soluble protein level (A/ G ratio) in OKC
fluid is low to those in serum.
 Thus the multilocular and loculated outlines
exhibited by OKCs were difficult to interpret on the
basis of unicentric hydrstatic expansion alone.
78

Role of inflammatory exudate in growth
of the cysts
 Inflammatory exudate has a negligible role in
OKC enlargement.
 The cyst walls are usually free of inflammatory
cell infilterate.
79

Role of glycosaminoglycans in growth of
the cyst
 GAGs, predominantly hyaluronic acid and also appreciable
amounts of heparin and chondroitin-4-sulphate, are present in
the fluids and walls of OKCs.
 Release of GAGs from the walls and their diffusion into the cyst
fluid increases the osmolality of the cyst fluid and hence raising
the internal hydrostatic pressure of the cyst.
80

 The epithelium of OKCs are relatively impermeable to high
molecular weight substances.
 Therefore the passage of GAGs into OKC fluid occur through
areas overlying foci of inflammation, where normal epithelial
structure is replaced by a non-keratinized stratified squamous
epithelium.
81

Bone resorption and growth
82
 But the evidence of parathyroid hormone related protein
(PTHrP) in OKCs has indicated less bone resorbing capacity.
 The PTHrP might modulate growth and bone resorption and
act synergistically with IL-1 to stimulate osteoblasts and
inhibit osteoclasts.

In 1967, Toller suggested that the OKC may best be regarded as
a benign neoplasm rather than a conventional cyst based on its
clinicalbehaviour.
 WHO reclassify the lesion as a tumour. Several factors form
the basis of this decision.
Behaviour: As described earlier, the KCOT is locally destructive
and highly recurrent.
Histopathology: Studies such as that by Ahlfors and others show
the basal layer of the KCOT budding into connective tissue. In
addition, WHO notes that mitotic figures are frequently found in
the suprabasal layers.
KCOT: The Neoplasm
JCDA • March 2008, Vol. 74, No. 2 • 83

Genetics: PTCH (“patched”), a tumour suppressor gene involved in
both NBCCS and sporadic KCOTs, occurs on chromosome 9q22.3-
q31.36–40 .
 Normally,PTCH forms a receptor complex with the oncogene SMO
(“smoothened”) for the SHH (“sonic hedgehog”) ligand. PTCH
binding to SMO inhibits growth-signal transduction.
 If normal functioning of PTCH is lost, the
proliferation-stimulating effects of SMO are permitted to
predominate.
84

PTCH prevents the proliferation-inducing effect of SMO
SHH releases PTCH from SMO, allowing signal .
JCDA. March 2008, Vol. 74, No. 2
85

Evidence has shown that the pathogenesis of NBCCS and sporadic
KCOTs involves a “2-hit mechanism,” with allelic loss at 9q22.42,43
The 2-hit mechanism refers to the process by which a tumour
suppressor gene is inactivated.
The first hit is a mutation in one allele, which, although it can be
dominantly inherited, has no phenotypic effect.
The second hit refers to loss of the other allele and is known as “loss of
heterozygosity” (LOH). In KCOTs, this leads to the dysregulation of
the oncoproteins cyclin D1 and p53.
Lench and others indicate that LOH in the 9q22.3-q31 region has
been reported for many epithelial tumours including basal cell
carcinomas, squamous cell carcinomas and transitional cell carcinomas;
they note that LOH is,“by definition a feature of tumorigenic tissue.”
JCDA • March 2008, Vol. 74, No. 2
86

Histopathology
Epithelial lining :
 Stratified squamous epithelium
 Parakeratinized – typically corrugated or wrinkled
 6 to 10 cells thick (uniformity of thickness of
epithelium)
 Prominent palisaded, polarized basal layers of cells
having picket fence or tombstone appearance.
 Epithelium often sloughs from connective tissue.
 No rete ridges unless secondary infected.
87

Cyst wall :
 Young fibroblast, seperated by stroma and
ground substance.
 Small islands of odontogenic epithelium and
daughter cyst (satellite cyst) are present.
88

Parakeratinized OKC Orthokeratinized OKC
More aggressive.
Associated with
syndrome.
Palisaded columnar
basal cell layer.
Less aggressive.
May be associated with
dentigerous cyst.
Flattened basal cell layer.
89

Odontogenic keratocyst epithelium exhibiting
characteristic loss of adhesion to underlying
connective
tissue. 90

Odontogenic keratocyst showing characteristic
parakeratinized lining with basal cell polarization.
91

Odontogenic keratocyst showing loss of characteristic
features in areas of inflammation, as well as mural
daughter cysts/rests
92

Odontogenic keratocyst. Note numerous positive
staining nuclei (brown) in immunohistochemical stain
for proliferation protein Ki-67.
93

Odontogenic keratocyst. Note numerous positive
staining cells (brown) in immunohistochemical stain for
antiapoptosis protein Bcl-2.
94

Orthokeratinized odontogenic cyst. Note granular layer
subjacent to keratin and lack of basal cell
organization.
95

Lateral Periodontal Cyst
 A slow growing, non-expansile developmental odontogenic
cyst derived from one or more rests of the dental lamina,
containing an embryonoic lining of one or three cuboidal
cells and distinctive focal thickenings (plaques).
 Those cysts that occur in the lateral periodontal position
and in which an inflammatory aetiology and a diagnosis of
collateral OKC have been excluded on clinical and
histological grounds.
96

Frequency :
Out of 3498 jaw cyst 24 Lateral Periodontal cyst
recorded in department of oral pathology of the
University of Witwatersrand, Johannesburg.
Age :
Peak frequency - 6th decade
Gender :
Male > Women (67:28 %)
Site :
Mandible > Maxilla
(bicuspid/cuspid/incisor) (maxillary lateral incisor)
98

 May be associated with a vital tooth
 Occasionally swelling
 Pain if infected
 Sometime discharge
99

 Unilocular radiolucency with a sclerotic margin.
 The cysts lay somewhere between the apex and the
cervical margin of the tooth .
Radiograph of a lateral periodontal cyst lying between
the mandibular premolar teeth. The margins are well
corticated, indicative of slow enlargement. (Courtesy of the
late Professor J.J.Pindborg.)
100

Pathogenesis
The possibilities which explain their origin and mode of
development include:
 Origin initially as a dentigerous cyst developing along the
lateral surface of the crown, and as the tooth erupts, the
cyst assumes a position in approximation to the lateral
surface of the root.
101

The possible pathogenesis of the lateral periodontal cyst.
102

 Origin from proliferation of rests of Malassez in the
periodontal ligament although the stimulus for this
proliferation is unknown.
 Origin from proliferation and cystic transformation of rests
of dental lamina, which are in a postfunctional state and
therefore have only a limited growth potential that is in
accordance with the usual small size of these cyst.
103

The possible mode of formation of epithelial plaques by
localised proliferation of cells.
(a) Cyst lined by thin epithelium resembling reduced
enamel epithelium.
(b) Early epithelial thickening by basal cell proliferation.
(c) Basal cells continue to proliferate.
Superficial cells swell by accumulation of intracellular
fluid.
104

(d) and (e) Basal proliferation ceases or slows down.
Superficial cells are waterlogged and swollen.
Plaque protrudes into cyst cavity and cyst wall where it
can undermine and raise adjacent cyst lining.
(f) Epithelial plaque can form convolutions. Protrusions
into cyst wall as in (c–f) may be ‘pinched off’ and
develop into daughter cysts, leading to the formation of
the botryoid variety of lateral periodontal cyst.
106

Histopathology
Epithelial lining :
 Stratified squamous epithelium (non-keratinized)
 One to five cell layers thick (resembles the reduced enamel
epithelium)
 Many of the lining cells have a clear, vacuolated, glycogen-
rich cytoplasm.
 Focal thickened plaques of proliferating lining cells often
projects into the lumen in areas.
 This lining is incomplete and easily sloughs away.
107

Cyst wall :
 The connective tissue subjacent to the epithelium exhibits a
zone of hyalinization, consisting of thick fibrous non-
inflamed cyst wall.
 Rests of dental lamina are sometimes found in the
connective tissue wall and these are often composed of
glycogen rich clear cell.
108

Lateral periodontal cyst. Note loculations lined by thick
and thin epithelium.
109

Lateral periodontal cyst which in part has a thin, nonkeratinised
stratified squamous epithelial lining resembling reduced enamel
epithelium. Two epithelial plaques are seen.
110

Part of the wall of a lateral periodontal cyst showing
multiple epithelial extensions ‘raining down’ from the
cyst lining.
111

BOTRYOID ODONTOGENIC CYST
• It is a variant of lateral odontogenic cyst, but that the term
‘botryoid odontogenic cyst’ should be retained because of the
tendency of this variant to recur if inadequately removed.
• Microscopically, the lesion is similar to the lateral periodontal
cyst but exhibits some differences.
• The lesion is multicystic with thin fibrous connective tissue
septa
112

• Growth can be seen as a clusters of grape [ botryoid] like
apperances.
• Site- mandible
• Radiographically – multilocular radiolucencies
• Clinical presentation- [ 5,6,7 Decades]
• Swelling
• Pain
• Discharge

114
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.

GINGIVAL CYST OF ADULTS
• A small developmental odontogenic cyst of the gingival soft
tissue derived from the rests of the dental lamina, containing a
lining of embryonic epithelium of cuboidal cells and distinctive
focal thickenings similar to the lateral periodontal cyst.
115

Age :
Peak frequency - 5th & 6th decade
Site :
Mandible > Maxilla
(premolar-canine region)
116

Oval, well-circumscribed swelling.
May occur in the free or attached gingiva or the
interdental papilla.
 Lesions are soft and fluctuant.
Adjacent teeth are usually vital.
117

Clinical photograph of a gingival cyst of an adult
118

Radiograph of a gingival cyst in an adult. There is a faint radiographic
shadow (marked with arrows) indicative of superficial bone erosion.
119

Pathogenesis
 It was originally proposed that they may arise
from odontogenic epithelial cell rests.
 By traumatic implantation of surface epithelium.
 By cystic degeneration of deep projections of
surface epithelium.
 Derived from glandular elements .
120

 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. 121

Low-power photomicrograph of a gingival cyst of the adult,
showing a very narrow epithelial cyst lining (bottom) deep
to the gingival epithelium. Part of the epithelial lining has
become detached. (Courtesy of Professor M. Altini and Dr
S.Meer.) 122

Narrow epithelial lining of a gingival cyst of the adult.
It resembles the reduced enamel epithelium found in
dentigerous cysts.
123

Gingival Cyst and Midpalatal Raphe Cyst of
Infants
 Bohn’s nodules are keratin-filled cysts scattered over
the palate,most numerous along the junction of the
hard and soft palate and apparently derived from
palatal salivary gland.
 Epstein’s pearls are cystic, keratin filled nodules
found along the mid-palatine raphe,probably derived
from entraped epithelial remnants along the line of
fusion.
124

 The lesions are small and white or cream
coloured .
 Frequency - high in newborn infants but they
are rarely seen after 3months of age.
 Most of them undergo involution and disappear,
or rupture through the surface epithelium and
exfoliate, as very few are submitted for
pathological examination.
125

Gingival cysts in an infant. (Courtesy of the Department
of Oral Medicine and Oral Pathology, University of
Copenhagen.)
126

Pathogenesis
• Gingival cysts in infants arise from the dental lamina.
• The epithelial remnants of the dental lamina, the so called
glands of Serres, have the capacity, from as early a stage
in development as 10weeks in utero, to proliferate,
keratinise and form small cysts.
127

 In the morphodifferentiation (late bell) stage of tooth
development, disintegration of the dental lamina occurred and
numerous islands and strands of odontogenic epithelium are seen
in the corium between the tooth germ and the oral epithelium,
remote from the developing alveolar process.
 Some of the gingival cysts probably open onto the surface leaving
clefts; others may be involved by developing teeth.
 Some degenerate and disappear, the keratin and debris being
digested by giant cells.
128

Gingival cysts in an infant. (Section
by courtesy of the late Dr W.G.
Shafer.)
Rests of Serres in the developing
alveolus of a human fetus. (Section
by courtesy of the late Professor
C.W. van Wyk.)
129

 The cysts along the midpalatal raphé have a different
origin.
 They arise from epithelial inclusions at the line of
fusion of the palatine shelves and the nasal
processes.
 This is normally completed by the 10th week.
 It was suggested the possibility that they may
represent abortive glandular differentiation leading
to cyst formation.
130

Midpalatal raphé cyst in a human fetus. Van Gieson
stain.
131

Histopathology
 The cysts are round or ovoid and may have a smooth or
an undulating outline .
 There is a thin lining of stratified squamous epithelium
with a parakeratotic surface and keratin fills the cyst
cavity, usually in concentric laminations containing
flattened cell nuclei.
 The basal cells are flat.
132

 Epithelial-lined clefts may develop between the cyst
and the surface oral epithelium.
 As a result of pressure from the cyst, the oral
epithelium may be atrophic.
 Midpalatine raphé cysts have a similar histological
appearance.
133

Glandular Odontogenic Cyst
(Sialo-Odontogenic Cyst)
 An unusually large solitary or multilocular
odontogenic cyst probably derived from the rests of
dental lamina, consisting of a stratified squamous
epithelium containing numerous mucus-secreting cells.
 It was first termed as ‘sialoodontogenic cysts’…
 This name was then replaced with GOC by the World
Health Organization (WHO)
134

Frequency :
Out of 3498 jaw cyst 06 Glandular Odontogenic cyst
Age :
Gender :
Male > Women (1.3:1)
Site :
Mandible > Maxilla
135

Size of lesion
 Dimension – 0.5 to 12 cm.
 Multilocular lesions are generally larger.
Semi quantitative evaluation of size in GOC
Lesions were classified as :
 Large lesions - if they involve area of bone larger than
occupied by 2 teeth.
 Small lesions – if they involve area of bone less than
occupied by 2 teeth.
136

Importance of semi quantitative evaluation of size
Size was found to be one of the features with correlation to the
aggressiveness and recurrence tendency of GOC.
86.5% of recurrent cases were classified as large lesions
64.3 % of these were both large and multilocular.
137

Clinical presentation
Lesion tend to cause expansion in most of the cases (88.5%).
Root resorption or tooth displacement were present in 22-
24% of cases.
Cortical plate integrity :
Cortical plate integrity is frequently compromised .
Of 41 cases reported
1. Perforation was reported in 61% of cases
2 .Thinning of plates in additional 24.4% of cases
Thus 85.4% of GOC cases encroach upon the cortical plate
This feature is an indication for aggressive potential of GOC
138

Radiographic characteristics
 Present as radiolucent lesions
 Lesions can be :
Multilocular : 53.8%
unilocular : 45.2%
with
Well defined borders - 95% &
Scalloped borders - 13%
139

Radiograph of a glandular odontogenic cyst in the
maxilla. There is a large unilocular radiolucent area with a
smooth corticated margin. These features are non-
specific.(Courtesy of Professor E.J. Raubenheimer.) 140

Radiograph of an extensive multilocular glandular
odontogenic cyst. (Courtesy of Professor C. Nortjé.)
141

Histopathology
 Diagnostic criteria has been divided
1.Major criteria
2.Minor criteria
 Focal presence of each major criteria is necessary
for diagnosis, while the minor criteria can support
the diagnosis but is not mandatory.
142

Major criteria
1. Squamous epithelial lining, with a flat interface with
connective tissue wall, lacking basal palisading.
2. Epithelium exhibiting variation in thickness along the
cystic lining with or without epithelial ‘spheres’ or
‘whorls’ or focal luminal proliferation.
3. Cuboidal eosinophillic cells or ‘hob nail’ cells.
4. Mucous (goblet) cells with intraepithelial mucous pools,
with or without crypts lined by mucous producing cells.
5. Intraepithelial glandular , microcystic or duct like
structures.
143

Minor criteria
I. Papillary proliferation of the lining epithelium.
II. Ciliated cells.
III. Multicystic or multiluminal architecture.
IV. Clear or vacuolated cells in the basal or spinous
layer.
144

cilia
Mucous cells
Squamous
epithelial lining
Intraepithelial microcyst
Hob nail cell
145

Histopatholgy of the glandular odontogenic cyst
146

Columnar and cuboidal cells lie on the surface of the
epithelium and extend into, and line, the intra-epithelial
crypts. The openings onto the surface give the epithelium a
corrugated appearance. (Histological section kindly lent by Dr
R. Morency.)
147

Glandular odontogenic cyst showing columnar or
pseudostratified columnar epithelium with mucus-
secreting goblet cells and filiform extensions of the
cytoplasm. Alcian blue stain 148

Calcifying Odontogenic Cyst (Calcifying Cystic
Odontogenic Tumor)
• ‘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 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.’
149

Suggested classification of the odontogenic ghost cell
lesions. (From Prætorius, 2006, personal
commmunication.)
 Group 1 ‘Simple’ cysts Calcifying odontogenic cyst
(COC)
 Group 2: Cysts associated with odontogenic hamartomas
or benign neoplasms: calcifying cystic odontogenic
tumours (CCOT). The following combinations have been
published:
• CCOT associated with an odontome
• CCOT associated with adenomatoid odontogenic tumor
• CCOT associated with ameloblastoma
150

 CCOT associated with ameloblastic fibroma
 CCOT associated with ameloblastic fibro-odontoma
 CCOT associated with odonto-ameloblastoma
 CCOT associated with odontogenic myxofibroma
151

 Group 3 :
• Solid benign odontogenic neoplasms with similar cell
morphology to that in the COC, and with dentinoid
formation. Dentinogenic ghost cell tumour
 Group 4 :
• Malignant odontogenic neoplasms with features similar
to those of the dentinogenic ghost cell tumour. Ghost
cell odontogenic carcinoma
152

Frequency :
Out of 3498 jaw cyst 28 Calcifying Odontogenic cyst
Age :
Gender :
Male = Women (negligible difference)
Site :
Maxilla > Mandible
(maxillary canine-premolar region)
153

 Swelling is most frequent.
 Pain if infected.
 Lingual expansion may sometimes be observed.
 Occasionally, the calcifying odontogenic cyst may
perforate the cortical plate and extend into the soft
tissues.
 Extraosseous lesions tend to be pink to red,
circumscribed elevated masses measuring up to
4cm in diameter.
154

 Unilocular radiolucency but a few have been multilocular.
 Regular outline with well-demarcated margins or may irregular and
may have poorly defined margins.
 Irregular calcified bodies of varying size and opacity may be seen in
the radiolucent area .
155

 Denser opacities are likely to be present if the cyst is
associated with a complex odontome.
 Root resorption of adjacent tooth .
 The extra-osseous lesions show localised superficial bone
resorption, or saucer-shaped radiolucencies.
156

Radiograph of a calcifying odontogenic cyst of the
maxilla. There is a well-demarcated margin and
calcifications suggestive of tooth material. (Courtesy of
Professor J.E.
Seeliger.)
157

Radiograph of a calcifying odontogenic cyst with well-
demarcated margins extending from the right to the
left premolar regions of the mandible. Numerous
calcifications are present, some suggestive of small
denticles. 158

Histopathology
Epithelial lining :
 The epithelial lining has prominent basal layer consisting
of palisaded columnar or cuboidal cells and
hyperchromatic nuclei which are polarised away from the
basement membrane.
 Budding from the basal layer into the adjacent connective
tissue and epithelial proliferations into the lumen are
frequently seen.
 Lining is six to eight cell layers thick.
159

Histological features of a calcifying odontogenic cyst with
clusters of fusiform ghost cells and focal calcifications, lying
in a stratified squamous epithelium 160

 The ghost cells are found in groups, particularly in the
thicker areas of the epithelial lining.
 The spinous cells in such situations may be widely
separated by intercellular oedema and the epithelium
around the ghost cells is often convoluted.
 The ghost cells are enlarged, ballooned, ovoid or elongated
elliptoid epithelial cells.
161

Theories of ghost cell formation
 During the development of CCOT, the transformation of an
odontogenic epithelial cell into a ghost cell firstly starts by
enlargement of mural cells (towards cystic cavity), followed by
other epithelial cells in cystic lining into abnormally keratinized
cells.
 The basal cells transform towards the end and this transformation
leads to loss of distinction between epithelium and connective tissue.
 Since ghost cells are abnormally keratinized they are considered as
foreign bodies if they reach the connective tissue.
 This theory was supported by Abrams and Howell.
162

 The possible pathogenesis of ghost cells in Odontomas, as
speculated by Levy, et al. (1973) was from metaplastic
transformation of odontogenic epithelium which occurs due
to reduced oxygen supply caused by walling-off effect by
the surrounding hard tissue calcification.
 When this continues, it can cause cell death and
keratinization.
 Thus, ghost cells are indicative of cell death from local
anoxia. This pathogenesis was later ruled out because of the
occasional presence of ghost cells in vicinity of blood
vessels 163

 Sam Pyo Hong,et al. (1991) suggested that ghost cells might be
the result of coagulative necrosis occurring at the same time
when CCOT undergoes liquefaction necrosis.
Ghost cells do not express reactivity for cytokeratins
but express for AE1/AE3 .
 This emphasizes their antigenic alteration which is probably due
to coagulative necrosis of the odontogenic epithelium in CCOT.
164

 Studies in Odontomas and CCOT revealed degenerating
cytoplasm consisting of numerous, short bundles of
tonofilaments
 Calcifications in the form of concentric layers; Liesegang’s
rings, was seen occurring on the outer surface of such cells
both on and between tonofilaments.
 Since degenerating foci is a prerequisite for dystrophic
calcification, this finding also reinforces the degenerating
nature of ghost cells.
165

Ghost cells with clear conservation of basic
cellular outline but lacking nuclear and
cytoplasmic details
Ghost cells undergoing calcifications
166

• They are eosinophilic with cell outlines are usually
well-defined.
• Sometimes it may 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.
• calcification may occur in some of the ghost cells, initially as fine
powdery or coarse basophilic granules and later as small
spherical bodies that ultrastructural studies have shown to
represent dystrophic calcification
167

Histological features of a calcifying odontogenic cyst with
clusters of fusiform ghost cells and focal calcifications, lying
in a stratified squamous epithelium 168

In this calcifying odontogenic cyst, there are sheets of ghost
cells and a focal area in which there has been induction of
a strip of dysplastic dentine (dentinoid).
169

A van Gieson stain distinguishes the red-staining
dentinoid from the yellow-staining ghost cells.
170

Cyst wall :
 The ghost cells may be in contact with the connective
tissue wall of the cyst where they may then evoke a
foreign body reaction with the formation on multinucleate
giant cells.
 In the fibrous wall there are usually strands and islands of
odontogenic epithelium, either in direct contact with the
epithelium or separately in the connective tissue.
171

 An atubular dentinoid is often found in the wall close to the
epithelial lining and often in relation to the epithelial
proliferations.
 Being found particularly in contact with masses
of ghost cells.
172

Radicular cyst
 Radicular cysts are the most common inflammatory cysts and arise
from the epithelial residues in the periodontal ligament as a rest of
periapical periodontitis following death and necrosis of the pulp.
174

Frequency :
Out of 3498 jaw cyst 1825 OKC recorded in department of oral pathology of the University
of Witwatersrand, Johannesburg.
Age :
Peak frequency - 3rd , 4th, 5th decade
Gender :
Male > Women
Site :
Maxilla > Mandible
Low in 1st decade and decline after 5th decade. As maxillary ant are
more prone to truma injuries may lead to pulp death. There is high
prevalance of palatal invaginations in the maxillary lateral incisors
and the frquency with which pulp death supervenes in these teeth.
175

 Associated with a non-vital tooth
 Swelling
 Pain
 Sometime discharge
 Multiple Radicular cyst – Hereditary dental defect (Multiple dens-
in-dente or dentinogenesis imperfecta)
 Not all non-vital tooth may form cyst as immune
mechanism may inhibit cyst formation
176

 Unilocular well-defined radiolucency
 Associated with non-vital tooth.
 Root resorption of adjacent tooth
177

Radiograph of a radicular cyst. The lesion is a
welldefined radiolucency associated with the apex of
a non-vital root filled tooth.
178

There are two types of radicular cyst:
 True radicular cyst: which contain a closed cavity
entirely lined by epithelium.
 The periapical pocket cyst (originally called the “bay”
cyst by Simon) in which the epithelium is attached to the
margins of the apical foramen in such a way that the cyst
lumen is open to the affected root cannel.
 The pocket cyst heal after RC t/t or tooth
extraction.
179

Pathogenesis
Pathogenesis of radicular cyst includes three phases:
 The phase of initiation
 The phase of cyst formation
 The phase of enlargement.
180

The phase of initiation
Rests of Malassez
In man, epithelial rest of malassez respresent in the
periodontal ligament as a network of cells
enmeshing the roots of the teeth (Simpson 1964).
In section they appear as islands close to the
cementum surface of the tooth. (Sicher 1962).
181

These cells are indeed resting:
Absence of mitotic figures
Their metabolism require little
energy
Absence of a developed Golgi
complex

 The lack of mitotic activity is due to presence of
intracellular, inhibitory chalone-adrenaline
complex.
 The altered environment of the periapical
granuloma would permit the release of these
inihibitors.
 Thus lead to renewal of mitotic activity.

Bacterial endotoxins released from the necrotic pulp.
Initiate the inflammation and immune response.
Results in epithelial proliferation.
185

Bacterial Endotoxin
Initiate inflammatory response
Results in production of cytokines(IL-1 and IL-6) with
pro-inflammatory and bone-resorbing activities
Have direct effect on epithelial proliferation.
186

Bacterial Endotoxin
Initiate immune response
Antigen-antibody complex and coactivate complement
Increased vascular permeability and a leucotactic response.
T-lymphocytes infilterate (as low complement component C3d
receptor activity, B-lymphocyte form only a minor component
of the mononuclear cells)
187

 Both humoral and cell-mediated immunological reactions in
response to egress of potential antigens from the root canal
system into the periapical tissue.
 T- helper cells predominated in most periapical granulomas
and cyst.
 Activated T-cells produced cytokines that may act on the
rests of Malassez causing proliferation and altered
differentiation leading to cyst formation.
188

Epithelial cells undergoes:
• Increase in cytoplasmic:nuclear ratio
• Increase pentose shunt metabolism
• Ribonucleoprotein synthesis.

Phase of Cyst Formation
 Degeneration of the central cells in thickening
processes of non-vascular epithelium.
 Degeneration of areas of granulation tissue
which have become surrounded by the
proliferating epithelial cells.

 The rest of Malassez proliferate and eventually form a
large mass of cells.
 With continous growth, the inner cells of the mass are
deprived of nourishment and they undergo liquefaction
necrosis.
 This leads to the formation of cavity which is located in
the center of the granuloma, giving rise to radicular cyst.
191

Potential mechanisms of bone resorption in
radicular cyst
193

Chloesterol Crystals
 If an unstained smear of cyst fluid is examined using a light
microscope, cholesterol crystals are seen to have a typical
rhomboid shape .
 In paraffin sections processed for routine H&E staining,
these crystals are dissolved by the fat solvents used in
dehydration and infiltration, leaving needle-shaped clefts
known as “cholesterol clefts” within cyst walls and
cavities.
 Notably, once cholesterol crystals have been deposited in
the cysts wall, they behave as foreign bodies and elicit a
foreign body giant cell reaction.
194

Theory of Cholesterol Crytal Formation
• Some authorities suggest that cholesterol clefts accumulate in
the tissues as a result of degeneration and disintegration of
epithelial cells (Thoma et al., 1970).
• M. Shear and others have on the other hand, suggested
circulating plasma lipids as a more likely source, as
cholesterol clefts are common in atherosclerotic plaques and
circulating lipids have been identified as the origin of
cholesterol in atherosclerosis
196

 (Browne, 1971) postulated that the main source of
cholesterol crystals was disintegrating erythrocytes.
 Approximately 55% of the erythrocyte membrane lipid is
phospholipid, while 42% is cholesterol and 3% comprise
glycolipids. Cholesterol in the erythrocyte membrane is
present in its free and non-esterified form (Best et al., 1985).
197

Histopathology
Epithelial lining :
 Stratified squamous epithelium (non-keratinized)
 Rarely lined by mucous producing epithelium (as result of
metaplastic transformation)
 Ruston bodies often found in great numbers in the epithelium.
198

Ruston bodies
Hyalin bodies appear as irregular, eosinophilic, glassy
structures, often with a granular center within the
epithelial lining and less frequently the CT wall of a
proportion of odontogenic cyst.
199

Theory of Rushton bodies formation
 One theory is that hyaline bodies are particular products of
odontogenie epithelium
(Wertheimer et al. 1962, Wertheimer 1966, Morgan & Johnson
1974, Morgan & Heyden 1975, Allison 1977a).
 Exclusive occurrence of hyaline bodies in odontogenic
cysts and the restricted presence within the epithelial lining
suggest a role of the odontogenic epithelium in the
formation process.
201

 Dewey (1918) considered that hyaline bodies might be
formed by hyaline degeneration of whole capillaries.
 Bouyssou & Guilhem (1965) and Sedano & Gorlin
(1968) suggested that hyaline bodies might originate
from thrombi in the capillaries.
202

 Homogenous types of hyaline bodies were occasionally
seen around the various structures, such as granular
material, mineralized masses, cholesterol clefts and so
on.
 Rushton considered granular material to be
degenerating cellular material whereby hyaline bodies
were deposited around granular material.
 Few author considered granular material as a precursor
of hyaline bodies
203

Hyaline bodies have some characteristic features:
 As to the lamellated structures, some authors considered
them as apposition lines .
(Morgan & Johnson 1974,Jensen & Erickson 1974).
 On the other hand, El-Labban (1979) suggested that they
may result from segregation of components within the
amorphous mass.
204

• The evidence suggests that hyalin bodies are a secretory
product of odontogenic epithelium deposited on the surface
of particulate matter, such as cell debris or cholesterol
crystals, in a manner analogous to the formation of dental
cuticle on the unerupted portions of enamel surfaces.
• There was no evidence in favor of either a keratinous or
hematogenous origin.
205

Cyst wall :
 Abundant fibroblast can be identified within cyst wall
 Lymphocytes and plasma cells are the most prominent.
 Erythrocytes , area of hemorrage, multinucleated
giant cells and cholesterol crystals are also present
206

Periapical cyst with a chronic inflammatory cell infiltrate
and nonkeratinized epithelial lining.
207

Pulse (seed) granuloma in the wall of a periapical cyst.
208

Specific stains
• PAS
• CD38
• CD138
• Papanicolaou ang Gomori
• Mallory aldehyde fuschin

Residual Cyst
 Retained periapical cysts from teeth that have been
removed.
 It could develop in a dental granuloma that is left
after an extraction.
210

 The residual cyst may present as a well-defined
radiolucency.
 Clinically, these cysts are usually found on routine
radiographic examination of patient.
 Become symptomatic upon secondarily infected.
211

Inflammatory Paradental Cyst
 The first detailed account of the paradental cyst was by
Craig (1976) who described a cyst of inflammatory origin
which occured on the lateral aspect of the roots of partially
erupted mandibular third molars where there was
an associated history of pericoronitis .
 He suggested that the term ‘paradental cyst’ was
appropriate for this lesion.
212

213
(a,b) Two cases of bilateral paradental cysts associated
with erupting mandibular third molar teeth. The cysts are
distal and buccal to the involved teeth.

Pathogenesis
 The cyst was of inflammatory origin, initiated by a
pericoronitis at the time of tooth eruption, and
considered rests of Malassez and reduced enamel
epithelium the most likely source of the cyst epithelium.
 The third molar lesions should be called‘eruption pocket
cysts’.
 It is possible that swelling associated with inflammation
leads to occlusion of the opening of the pocket, thus
allowing accumulation of debris and cyst growth by
osmotic pressure in a similar process to that described
for radicular cysts 214

Histological features
 The cysts are lined by a hyperplastic, non-keratinised,
stratified squamous epithelium.
 An intense inflammatory cell infiltrate was present
associated with the hyperplastic epithelium and in the
adjacent fibrous capsule.
215

216
Paradental cyst adjacent to the root of an impacted
mandibular third molar. The cyst is lined by non-keratinised
stratified squamous epithelium of variable thickness and
showing areas of proliferation (H & E). (By courtesy of Dr G.T.
Craig.)

217
Part of the lining of a paradental cyst showing
proliferative epithelium and cholesterol clefts (H & E). (By
courtesy of Dr G.T. Craig.)

Conclusion
o In summary, there are a multitude of odontogenic cysts
that may present in head and neck patients. The key to
diagnosis is a careful history and physical examination
accompanied by radiographic evidence and pathologic
confirmation.
o Many of these entities represent benign lesions, however
significant pathologic disease may be lurking which
necessitates prompt treatment and immediate consultation
as necessary.
218

References
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8. P. R. MORGAN;Histological, histochemical and ultrastructural
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220

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