Mohammed Zaki Lohar et al.

URJDS 2014, 01 (01): Page 10--17

Review Article

UNIVERSAL
RSAL RESEARCH JOURNAL OF DENTAL SCIENCES
Available online: www.ujponline.com

ODONTOGENIC KERATOCYST AT A GLANCE: A REVIEW ARTICLE

Mohammed Zaki Lohar11*, Mohd Adhnan MF2, Shahid Khan3, Mohammed Shafi Lohar4
1

MDS, Royal Multi-Speciality

Speciality Dental Clinic & Implant Centre, Royal Touch Complex, Ganesh Peth, Hubli, Karnataka, India
2
MDS, Opp Gajanan M
Mandir, Nagpur Road, Chandrapur, Maharashtra, India
3
MDS, House no 2, Shakti Ward, Kawardha, Chattisgarh, India
4
BDS, Royal Multi-Speciality
Speciality Dental Clinic & Implant Centre, Royal Touch Complex, Ganesh Peth, Hubli, Karnataka, India

Received 24-10
10-2014; Revised 22-11-2014; Accepted 20-12-2014
1

*Corresponding Author
Author: Dr Mohammed Zaki Lohar,
MDS, Royal Multi-Speciality
Speciality Dental Clinic & Implant Centre, Royal Touch Complex, Ganes
Ganesh Peth, Hubli, Karnataka, India,, Mobile Number-09743904346
Number

ABSTRACT
The purpose of this paper is to review the features and behavior of the odontogenic keratocyst (OKC), now officially known as the
keratocystic odontogenic tumor (KCOT) to analyze a series of histologically con
confirrmed
rmed KCOT cases; and to review and discuss the
redesignation of KCOT and thee implications for treatment. Based on a literature review, this article enlightens about the epidemiology,
its location, clinical, radiological and histological features, immuno
immuno-histochemistry,
histochemistry, reasons for reclassification into KCOT, different
treatment modalities,
odalities, recommended protocols in management and reasons for recurrences.
Keywords: Odontogenic Keratocyst (OKC), Keratocystic Odontogenic T
Tumor (KCOT)

INTRODUCTION
Odontogenic keratocysts (OKCs) are developmental
odontogenic cysts of epithelial origin, first identified and
described in 1876 and further characterized by Phillipsen in
1956 is defined as a benign uni or multicystic, intraosseous
tumor of odontogenic origin, with a characteristic lining of
parakeratinized striated squamous epithelium and potential for
aggressive, infiltrative behaviour1,2. Pindborg and Hansen
suggested the histological criteria necessary to diagnose OKC
in 1962. The initial terminology for an odontogenic keratocyst
(OKC) was "primordial
ordial cyst". And renamed as "odontogenic
keratocyst by World Health Organization (WHO) in 1992
based on histologic typing. Recently the cyst has been
reclassified into benign neoplasm (KCOT).
Histopathologically OKC/KCOT typically shows a thin,
friable wall, which is often difficult
ficult to enucleate from the bone
in one piece, and have small satellite cysts within the fibrous
wall. Therefore odontogenic keratocysts often tend to recur
after treatment3.
The treatment of the OKC/KCOT remains controversial.
Treatments are generally classified
fied as conservative or
aggressive. Conservative treatment generally includes simple
enucleation, with or without curettage or marsupialization.
Aggressive treatment generally includes peripheral ostectomy,
chemical curettage with Carnoys solution, cryotherapy, or
electrocautery and resection4, 5.
The choice of treatment should be based on multiple factors;
patient age, size and location of the cyst, soft tissue

involvement, history of previous treatment and a histological

variant of the lesion. The goal is to choose the treatment
modality that carries the lowest risk of recurrence and the least
morbidity6.
Epidemiology
Odontogenic keratocysts (OKCs) account for approximately
3-11%
11% of all cysts in the jaws. They occur in all ages, with a
peak incidence in the second and fourth decades of life, with
the youngest patient reported at age 5 years.
Etiology
Odontogenic keratocysts (OKCs) are generally thought to be
derived from remnants of the dental lamina (rests of Sere),
traumatic implantation or down growth of the basal cell layer
of the surface epithelium, or reduced enamel epithelium of the
dental follicle. Studies have suggested a genetic cause,
specifically a PTCH gene aberration, in the etiology of these
cysts.
Location
Odontogenic keratocysts (OKCs) can be found in the
mandible and the maxilla but are twice
twi as common in the
mandible, with a predilection for the angle and ascending
ramus. Rare examples of these cysts arising from the
temporomandibular
joint(TMJ)
have
been
reported. Mandibular cysts can cross the midline, and
maxillary cysts may involve the sinus and floor of the nose.
Although most odontogenic keratocysts (OKCs) are
encountered as intra-osseous
osseous lesions, peripheral manifestations
have been reported, primarily involving the buccal gingival
ging
soft tissue in the canine area of the mandible.

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Clinical and Radiological Features
Clinically, odontogenic keratocysts (OKCs) generally present
as a swelling, with or without pain. The cyst classically grows
within the medullary spaces of the bone in an anteroposterior
direction, causing expansion that is at first minimal. Buccal
expansion is noted in approximately 30% of maxillary and
50% of mandibular lesions. It has been demonstrated that the
collagenase activity in the cysts' epithelium with its
resorbative properties appears to regulate the ability of the
lesion to grow expansively in bone.
Radiographically, odontogenic keratocysts (OKCs) present as
a well-defined radiolucent lesion that is either unilocular or
multilocular, with smooth and usually corticated margins,
unless they have been secondarily infected. In 25-40% of
cases, there is an unerupted tooth involved with the lesion ,
adjacent teeth may be displaced, but root resorption is rarely
seen. Maxillary lesions tend to be smaller than mandibular
lesions; however, more extensive involvement can be
appreciated in the maxilla because of the cancellous nature of
the bone. Larger lesions can cause bony expansion with or
without perforation of the cortical plates.

expansion. The scalloped margin of a simple bone cyst and its

tendency for minimal expansion can be similar to that of an
odontogenic keratocysts (OKCs); however, the margins of a
simple bone cyst are more delicate and difficult to detect.
Keratoameloblastoma, a rare histologic variant of the
ameloblastoma, can resemble an odontogenic keratocyst
(OKC). The epithelium lining of keratoameloblastoma differs
from the OKC in that it is not always of uniform thickness,
and there is typically separation and edema between the basal
cell layer and the rest of epithelium in the
keratoameloblastoma.
Gross Findings
The epithelial lining and connective tissue wall of the
odontogenic keratocyst (OKC) is characteristically thin and
friable, thus causing the specimen to fragment when
treated. Grossly, the lesion often has a bosselated, gray, cystic
appearance mimicking the appearance of a glove.
Microscopic Findings
In 1962, Pindborg and Phillipsen and Henriksen established
strict histologic criteria for the diagnosis of an odontogenic
keratocyst (OKC). These criteria include an epithelial lining
that is usually thin and uniform in thickness, with little or no
evidence of rete ridges; a well-defined basal cell layer, the
component cells of which are cuboidal or columnar in shape
and often fashioned in a palisaded arrangement; a thin,
spinous cell layer which often shows a direct transition from
the basal cell layer; spinous-cell layer intracellular edema;
surface keratinization that is corrugated and predominantly
parakeratotic; and a fibrous connective tissue cyst wall that is
thin and usually uninflamed .

Figure 1: Computed tomography scan a multilocular odontogenic

keratocyst. demonstrating extensive compartmentalization of
mandibular odontogenic keratocyst.

Radiographically, differentiation between an odontogenic

keratocyst (OKC) and other odontogenic cysts and tumors can
be challenging. The radiographic features of odontogenic
keratocysts (OKCs) are not pathognomonic, and the
presentation can be similar to that of other odontogenic cysts
and tumors. Odontogenic keratocysts (OKCs) can present as
dentigerous cysts, primordial cysts, residual cysts, lateral
periodontal cysts, or cysts in a nasopalatine location.
Misinterpretation of an odontogenic keratocyst (OKC) as a
lesion of endodontic or periodontal origin can confuse
treatment planning .to diagnosis (see.
When odontogenic keratocysts (OKCs) are seen in a
pericoronal location, differentiation from a dentigerous cyst
may be difficult. Radiographic connection of a cyst to a tooth
at a point apical to the cement enamel junction, with no
expansion, favors an odontogenic keratocyst (OKC). The
typical multilocular appearance of an OKC can be mistaken
for that of ameloblastoma or odontogenic myxoma, although
ameloblastomas typically present with significant clinical

Figure 2: Typical odontogenic keratocyst lining.

Additionally, satellite cysts, solid epithelial proliferations,

odontogenic rests (see the image below), and basal layer
budding have been described in association with the
odontogenic keratocyst (OKC). The incidence of daughter
cysts in the cyst wall is reported to range from 7% to 30.1%.
Mineralization in the fibrous connective tissue wall may
occur, along with inclusion of cholesterol crystals and Rushton
bodies.
A number of studies have discussed the histologic variants of
the odontogenic keratocyst (OKC): (1) Parakeratinized (2)
Orthokeratinized (see the second image below) and (3)
combined. There appear to be no statistical differences
between orthokeratinized and parakeratinized odontogenic

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keratocysts (OKCs) when age, race, sex, symptomatology, and
the clinical impression are compared. The recurrence rate,
however, is much higher in the parakeratinized variant, thus,
some investigators have suggested that the orthokeratinized
variant be classified as a separate entity.
Immunohistochemistry
Strong p63 staining has been demonstrated in the epithelium
of odontogenic keratocysts (OKCs), especially in the
suprabasal layer of the epithelium. It has been postulated that
p63 plays a role in blocking apoptosis-inducing and growth
inhibitory actions, which may facilitate the proliferative
potential of epithelial cells due to its capability of blocking
wild type p53, thus enhancing the biologic aggressiveness of
these cysts.
Matrix metalloproteinases (MMPs) are enzymes thought to
play an important role in regulating the integrity and
composition of the extracellular matrix (ECM) and
consequently degradation, proliferation, differentiation, and
cell death. MMP-1s expression is thought to be associated
with odontogenic keratocyst (OKC) degradation of the organic
bone matrix, favoring dissemination of these cysts through the
trabecular spaces. With immunohistochemistry, MMP-2s have
also been observed to reside in the basement membrane of
odontogenic keratocysts (OKCs), and they have been
implicated in the degradation of the extracellular matrix
surrounding the cysts.
Vascular endothelial growth factors (VEGFs) comprise a
family of multifunctional proteins and act as a sensitive
measure of the angiogenic potential of a lesion. VEGFs have
been implicated in the pathogenesis of cystic tumors and
radicular cysts and they have been documented to be intensely
expressed in odontogenic keratocysts (OKCs).
Contents of Cyst
Heparin sulphate, chondroitin 4 sulphate, Hyaluronicacid,
GAG. On aspiration there it is whitish, cheesy material with
keratin flecks. There is low protein content (< 4mg/dl) with
specific gravity 1.018.
Odontogenic Keratocysts (OKC) Reclassified as
Keratocystic Odontogenic Tumor (Kcot)
The odontogenic Keratocyst is regarded as a developmental
abnormality and is generally known for its aggressive nature
and high recurrence rate, especially in comparison with other
developmental odontogenic cysts. In addition to a distinctive
clinical aggressive biological behavior, the expression of
various proliferation markers in the epithelial lining and over
expression of p53 protein and mutations in p53 and PTCH
genes (tumor suppressor genes) have led several investigators
to consider odontogenic keratocysts as a benign cystic
neoplasm.
The components of the connective tissue in KCOT revealed
some resemblance with the stromal myofibroblasts,
differences in the collagen fibers of the extracellular matrix
,high
enzymatic
activity
with
increased
matrix
metalloproteinases (MMPs) and mast cell tryptase and
increased expression of receptor activator of nuclear factor-kB
(RANK), RANK lig-and (RANK), RANK LIG- and
(RANKL), osteoprotegerin (OPG) and tumor angiogenesis,
Focusing on the importance of the epithelial mesenchymal

interactions in odontogenic tumors, previous studies supported

that the stroma of keratocysts should not be regarded just a
structural support of the cyst wall, but rather as portraying the
features of atumoral stroma.
However, its growing potential to a large size before
manifesting clinically and the tendency to recur following
surgical treatment, give rise to a discussion as to its true
pathological nature and terminology. Hence in 2005 World
Health organization ,based on behavior ,histology and
genetics, reclassified the traditional designation ,stressing the
benign behavior of this lesion was substituted by a term that
would better reflect its neoplastic nature Keratocystic
odontogenic tumor (KCOT) and the lesion was thus described
as benign uni or multicystic, intra-osseous tumor arising from
the dental lamina or its remnants. The orthokeratinized variant
of the odontogenic keratocyst is not currently included as
being part of the spectrum of keratocystic odontogenic tumor.
The main histopathological features defined in 2005 enable to
differentiate KCOT from jaw cysts with keratinization.
Well defined, oftenpalisaded, basal layer of columnar cuboidal
cells.
Intense basophilic nuclei of the columnar basal cells oriented
away from the basement membrane.
Parakeratotic layers with an often corrugated surface
Mitotic figures frequently present in the suprabasal layer
Management
1. Decompression and marsupialization
Decompression of a cyst involves any technique that relieves
the pressure within the cyst as this pressure is the way by
which the cyst grows by expansion. Decompression can be
performed by making a small opening in the cyst and keeping
it open with a drain3,7.
Marsupialization, on the other hand, involves converting the
cyst into a pouch so the cyst is decompressed, but this is a
more definitive treatment than decompression as it exposes the
cyst lining to the oral environment. Mandibular cysts are
normally marsupialized into the oral cavity, while maxillary
cysts can also be marsupialized into the maxillary sinus or
nasal cavity, as well as the oral cavity7,9.
Decompression and marsupialization of cysts is probably the
earliest recommended treatment and was first suggested by
Partsch in the late 19th century. In many parts of the world,
marsupialization is still described as a Partsch I procedure (the
Partsch II procedure is enucleation and primary closure) 10,11.
Although decompression or marsupialization was not
recommended as treatment for the KCOT by some authors,
because it was thought that the pathologic tissue would be left
in situ7, decompression or marsupialization has been
recommended in a number of studies as a technique that
allows partial decrease in size in the KCOT so that vital
structures like teeth or the inferior alveolar nerve can be
preserved, then the KCOT was certainly enucleated 7,11.
Those authors who are against the use of marsupialization or
decompression for the treatment of KCOT depend on, that this
technique does not remove completely the whole cystic
covering, which would lead to a continuation of epithelial
proliferation and facilitate the13,14. Brondum and Jensen (1991)
reported a recurrence rate of 25% in 32 (OKCT) patients

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treated with decompression of the lesion. On the other hand,
other studies have shown that marsupialization of KCOT can
be followed by total resolution of the lesion without any
further surgery7,8.
The marsupialization technique was described by
Pogrel(2005) as a window at least 1 cm in diameter is made
into a cyst, and an attempt is made to suture the cyst lining to
the oral mucosa. In the maxilla, the cyst is then often packed
open with the packing protruding through the opening. The
packing consists of iodoform gauze impregnated with
bacitracin ointment. When it is removed in the maxilla, the
cavity is usually self retaining and the patient needs to irrigate
twice a day to prevent food accumulation or closure of the
fistula. In the mandible, there is a greater tendency for
spontaneous closure of the fistula and reformation of the cyst,
particularly in the posterior mandible. In these cases, we have
found that the use of a nasopharyngeal anaesthesia tube
suitably cut down makes an excellent stent to keep the cyst
open. Again, the cavity is irrigated twice daily7.
Studies have shown that when the OKCT is open to the oral
cavity by marsupialization, a number of changes occur in the
cyst lining. Histologically, the lining of OKCT is only 5 or 6
cells thick and tears easily on attempted enucleation; which is
one of the causes of the high recurrence rate. With
decompression or marsupialization, the lining appears to
become thicker and easier to enucleate, and histologically it
does appear to change and resemble normal oral mucosa, both
with routine histology and with immunohistochemistry 7,15.
Pogrel (2005) concluded that, decompression and/or
marsupialization has at least as high a success rate as the other
more aggressive treatments with lower morbidity and
preservation of important vital structures7.
2. Enucleation with and without adjuncts
To enucleate is to remove whole or clean, as a tumour from
its envelope. Curettage is defined as the removal of
growths or other material from the wall of a cavity
Enucleation with and without various adjuncts has been
utilized for many years. Although enucleation/curettage has
the advantage over marsupialization of providing a complete
specimen for histopathologic analysis, it shows recurrence
rates as high as 62.5%, which is no longer an acceptable
treatment modality. This high incidence of recurrence is
explained by the thin, friable wall of the OKCT, which is often
difficult to enucleate from the bone in one piece, and the small
satellite cysts within fibrous wall. Many clinicians consider
enucleation and curettage as the minimal requirement in the
treament of KCOT7,16. Regarding curettage, clinicians have
advocated mechanical techniques (hand, rotary) alone or in
combination with a chemical solution (Carnoys) (Stoelinga,
2003) or cryosurgical agents (liquid nitrogen) 7,16.
3. Enucleation and treatment of the bony defect with
Carnoy solution
As a result of the difficulty of enucleating the thin, friable wall
of the KCOT as one piece, and due to the small satellite cysts,
therefore, treatment should aim to eliminate the possible vital
cells left behind in the defect. For this reason a mild, not
deeply penetrating, cauterizing agent is used such as Carnoys
solution {consists 3 ml of chloroform, 6 ml of absolute

ethanol, 1 ml of glacial acetic acid and 1 g of ferric chloride}4.

This should be enough to do cauterization of the remaining
cells. In case the cyst has penetrated through the lingual or
buccal cortex, authors described the use electro-cauterization
to avoid a recurrence in the soft tissues19.
Other studies showed that, although the defect was treated
with Carnoys solution. Microcysts and epithelial islands were
always seen in the overlying attached mucosa. And so
recursence took place. So, the authors of these studies
recommended the complete excision of the overlying mucosa
to decrease the recurrence 18,20. also reported in their study that
the treatment with Carnoys solution did not show a significant
association with recurrence4. Yet, Voorsmit et al. (1981)
reported a decreased recurrence rate following treatment with
enucleation and Carnoys solution (2.5%) compared with
enucleation alone (13.5%). According to enculation of KCOT
followed with application of Carnoys solution appears to be
the least invasive procedure with the lowest recurrence rate.
And they reported that adding Carnoys solution to the cyst
cavity for 3 min after enucleation results in a recurrence rate
comparable to that of resection without unnecessarily
aggressive surgery 21.
The effects of Carnoys solution on the inferior alveolar nerve
were first reported 21. The authors did not observe axonal
damage during the first three minutes of direct application. In
contrast, another important study, Wolgen et al. (1999), noted
that the alterations in neural conductivity developed after 2
min of direct application, with few signs of recovery after two
weeks of follow-up. However, Ju nior et al. (2007), reported
that when a proper protocol is followed, the chemical
treatment of the nerve can be accomplished without permanent
functional damage.
4. Enucleation and liquid nitrogen cryotherapy
Theoretically, the ideal treatment for the KCOT would be
enucleation or curettage followed by treatment of the cavity
with an agent that would kill the epithelial remnants or
satellite cysts. In addition, the osseous framework should be
left intact to allow for osteoconduction. Liquid nitrogen has
the ability to devitalize bone in situ while leaving the
inorganic frame work untouched, as a result of this,
cryotherapy has been used for a number of locally aggressive
jaw lesions, including KCOT, ameloblastoma and ossifying
fibroma. Cell death with cryosurgery occurs by direct damage
from intracellular and extracellular ice crystal formation plus
osmotic and electrolyte disturbances 23.
According to Schmidt and Pogrel (2001) the standardized
technique is as follows, the initial step in management of the
lesion is enucleation of the cyst. The surrounding tissues are
then protected with sterile wooden tongue blades and gauze,
and the cavity is sprayed with liquid nitrogen twice for 1 min,
with a 5-min thaw between freezes. Bone graft can inserted in
the defect simultaneously, and then mucosa is closed with
watertight sutures7,23.
The advantages of liquid nitrogen over alternative methods of
devitalizing the tissue beyond the visible lesion of the margin
are that
(1) The bone matrix is left in place to act as a clean scaffold
for new bone formation,

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(2) A bone graft can be placed immediately to accelerate
healing and minimize the risk of a pathologic fracture, and
(3) decrease of bleeding and scarring.
However, because of the difficulty in controlling the amount
of liquid nitrogen applied to the cavity, the resultant necrosis
and swelling can be unpredictable. The recurrence rate
following enucleation and liquid nitrogen cryotherapy has
been reported at 39% 7,24.
When the liquid nitrogen cryotherapy is given around the
inferior alveolar nerve, it is affected, and patients will suffer
paraesthesia or anaesthesia. However, the axon sheaths are left
intact and nerve regrowth is normal such that most patients
obtain partial or complete return of sensation in 3 months7,24.
Block resection, with or without preservation of the continuity
of the jaw Resection refers to either segmental resection
(surgical removal of a segment of the mandible or maxilla
without maintaining the continuity of the bone) or marginal
resection (surgical removal of a lesion intact, with a rim of
uninvolved bone, maintaining the continuity of the bone)
which is an extreme technique, that results in considerable

morbidity, particularly because reconstructive measures are

necessary to restore jaw function and aesthetics18,19,20, wonders
whether such aggressive therapy is warranted for a benign
lesion that can be managed reasonably well with relatively
simple means. In a systematic review done by Blanas et al.
(2000)21, the authors reported that resection was found to have
the lowest recurrence rate (0%) but the highest morbidity rate,
while enculation with application of Carnoys solution can
result in a recurrence rate comparable to that of resection
without unnecessarily aggressive surgery. Multiple studies
concluded that keratocysts might be treated with a
conservative approach, the only disadvantages being the
extended therapeutic time. Extensive resection of the mandible
with its attendant morbidity may be too radical for large
KCOT and even an overtreatment16.
Decision Tree
The decision trees on the treatment of cystic lesions of the
jaws based on their location. Special consideration was given
for the treatment of potentially aggressive lesions such as
odontogenic keratocysts and cystic ameloblastomas18,19,20.

Figure 3: Protocol for management of uni-locular cystic lesion maxilla and body of mandible.

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Figure 4: Protocol for management of multi -locular cystic lesion.

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Figure 3: Protocol for management of uni

uni-locular
locular cystic lesion involving retromolar trigone and ascending ramus.

Recurrences25,26
The incidence of recurrence of OKC has varied from 2.5% to
62%.The great degree of variation in these report
reports are mainly
because some series included cysts from patients with Nevoid
Basal cell carcinoma syndrome (NBCCS), while other reasons
for this variation can be due to duration of the follow
follow-up
period
and
method
of
treatment
used.
In 1976, Brannon proposed three
hree mechanisms for OKC
recurrence: Incomplete removal of the cyst lining, growth of a
new OKC from satellite cysts (or odontogenic rests left behind
after surgery), and development of a new OKC in an adjacent
area.
Histopathological features that predict recurrences.
The major features that can be considered to predict
recurrences in OKC are
Higher level of cell proliferative activity in the epithelium
Budding in the basal layer of the epithelium
Parakeratinization of the surface layer

Supraepithelial splitt of the epithelial lining

Subepithelial split of the epithelial lining
Presence of remnants/cell rests as well as daughter cysts.
Summary
OKC/KCOT is one of the most aggressive odontogenic lesion
with a high recurrence rate. Multiple surgical approaches were
introduced including decompression, marsupilization,
enucleation with or without adjunct (Carnoys solution,
cryotherapy) and resection. Depending on other studies KCOT
can be conservatively treated with enculation and application
of Carnoys solution or cryotherapy. This can be used
specially in the large lesions that when treated with resection,
the continuity of the jaw will be interrupted. This technique
shows comparable results to other more aggressive techniques.

ACKNOWLEDGEMENT
The author is very
ry much thankful to Dr.
Dr Asif Karigar for his
kind support.

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Source of support: Nil, Conflict of interest: None Declared

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