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Pathogenesis of Odontogenic Cysts

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Pathogenesis of Odontogenic Cysts

Neeharika Mortha1, Divya Uppala2

Abstract
Context: Although, there is abundance of literature available on their nature, character and treatment modalities, the exact
pathogenesis still remains under continual scrutiny.
Objective: Cysts of oral cavity are a subject of importance to pathologists and practising dental surgeons hence needs to be
reviewed.
Materials and Methods: Two reviewers independently collected data from books, case reports and review articles published
in electronic databases including Google search, Research gate, Pub Med and Science Direct.
Result and Conclusion: This article summarizes the concepts put forth by a number of investigators to explain the pathogen-
esis of Odontogenic Cysts and their causation mechanisms, thus enhancing our understanding.
Keywords: Cavity; Egg-shell; Globulin; Osmosis.
Oral and Maxillofacial Pathology Journal (2021): http://www.ompj.org/archives.

Introduction 1
Visakha Institute of Medical Sciences, Visakhapatnam, Andhra
Cysts occur in the jawbones and soft tissues, categorized as
Pradesh, India, 2Department of Oral & Maxillofacial Pathology,
those arising from tooth forming tissues and non-tooth forming
GITAM Dental College and Hospital, Visakhapatnam, Andhra
tissues, namely Odontogenic and Non-Odontogenic cysts with
Pradesh, India.
the Odontogenic being most common.1 Most of the Odonto-
genic cysts are lined by epithelium derived from Odontogenic Corresponding author: Neeharika Mortha, Visakha Institute
epithelium. These cysts are again categorized as Developmental of Medical Sciences, Visakhapatnam-530 040, Andhra Pradesh,
and Inflammatory Cysts. Modifications in their classifications and India. Contact: 9948777396, e-mail: neeharika.riviera@gmail.com
terminologies were made over the years since 1868 with the ad- How to cite this article: Mortha N, Uppala D. Pathogenesis of
dition of newer concepts and deletion of old ideas. In 2017 the Odontogenic Cysts. Oral Maxillofac Pathol J 2021;12(1): page no.
4th edition of the World Health Organization’s Classification of 31-34
Head and Neck Tumours was given to enable the diagnosis of Source of Support: Nil
Odontogenic cysts, tumours and other allied bone tumours.1,2
Conflict of Interest: None
The changes in the classifications aid in better understanding of
the pathogenesis of the cysts.
The Inflammatory Odontogenic cysts are: Radicular Cyst and cephalic neural crest and, the first pharyngeal arch ectoderm,
Inflammatory Collateral Cyst. The Developmental Odontogenic leading to the dental mesenchyme formation, the dental pulp,
cysts are: Dentigerous Cyst, Odontogenic Keratocyst, Lateral odontoblasts, dentine matrix, cementum and periodontium.4 The
Periodontal Cyst And Botryoid Odontogenic Cyst, Gingival Cyst, whole event is a nexus involving induction, proliferation, differen-
Glandular Odontogenic Cyst, Calcifying Odontogenic Cyst and tiation, morphogenesis, and maturation regulated by signalling
Orthokeratinized Odontogenic Cyst. These cysts are usually as- molecule families leading to the formation of a primary dental
ymptomatic, with the potential to become extremely large caus- lamina as a thickening of oral epithelium.5,6 The mesenchymal tis-
ing cortical expansion and erosion, while some can be aggres- sue surrounding this developing enamel organ responds by pro-
sive, with jaw destruction or can be frequently recurrent.3 Both liferation to form a dense mass of cellular tissue, the dental papilla
developmental and inflammatory types, share a nearly identical and the follicular sac for each tooth bud.7 Conserved signalling
cytomorphology. Therefore, unravelling mechanisms of tooth molecules regulate the differentiation process of the ameloblasts
development provides insights into the pathogenesis of these from the epithelium, odontoblasts and cementoblasts from mes-
Odontogenic cysts. enchyme which later deposit the matrices of enamel, dentin and
cementum respectively. A large portion of this epithelial tissue is
Inciting Factors lost during the tooth eruption process.4,6 The remnants of dental
Tooth development is an event filled process marked by in- lamina may persist as Epithelial pearls or islands within the jaw &/
teractions between the ectomesenchymal cells originating from or gingiva. Odontogenic cysts arise from these cellular remnants
© The Author(s). 2021 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.
org/licenses/by-nc-sa/4.0/), which permits unrestricted use, distribution, and non-commercial reproduction in any medium, provided you give appropriate credit to
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 Pathogenesis of Odontogenic Cysts

of post-functional state of dental lamina entrapped within the epi- their nutritional supply and undergo liquifactive necrosis resulting
thelial remains of the Malassez or the gingiva named epithelial rests in cystic cavity (Nutritional deficiency theory). When an abscess
of Serres or either arises from the accumulation of fluid between cavity is formed in the periapical connective tissues, it becomes
the reduced enamel epithelium of the dental follicle and the crown surrounded by epithelium because of the natural inclination of the
of the unerupted tooth.8 The presence of abundant epithelial rem- stratified squamous epithelium to line exposed connective tissue
nants in the jaws makes the prevalence of cysts higher in the jaws surfaces (Abscess theory). Each epithelial cell rest proliferates due
than any other human body part.9,10,11 to cytokine and growth factor stimulation in the inflammatory en-
vironment to form epithelial cell strands that are polarized. Under
Pathogenesis suitable conditions and with time the strands merge, wrapping the
Shear (1960) documented that, cysts arising from cell rests abscess or foreign debris to become cysts. The cysts continue to ex-
gave rise to simple epithelial linings which increase in size gradu- pand under persisting growth stimulus, allowing the basal cell to
ally due to degenerative characteristics of their linings, with rise in grow and expand (Merging of epithelial strands theory).25 The pro-
osmolality of the cyst contents. The absence of lymphatic access is liferative epithelial strands as a result decomposition of epithelial
thought to be fundamental to sustained cyst growth. In contrast, and granulation tissue and simultaneous convergence of multiple
cysts derived from epithelial residues of the dental lamina which cavities serve as a scaffold for development of cyst wall. Some state
is non-contributory to a stable tooth structure are most likely to that inflammations in the apical region of non-vital teeth or peri-
be lined by a keratinizing membrane, showing the characteristics apical granulomas are caused by bacterial endotoxins which serve
of cell maturation rather than degeneration. They may increase as mitogens for epithelial cells and as a stimulus for cytokine pro-
in size predominantly by process of epithelial cell multiplication. duction. Investigators found that the decomposition of epithelial
These two types of cysts exhibit different clinical behaviour, as well cells, leukocytes and the accumulation of plasma exudates cause
as fundamental differences in the activity of their epithelial lin- increased gamma globulin levels than the patients serum, thus in-
ings at the cellular level.12 Harris, mentions the odontogenic cyst ternal hydrostatic pressure becomes more significant than capillary
growth occurs with resorption of the surrounding bone and with pressure leading to diffusion of tissue fluids into the cyst. Therefore,
accumulation of intracystic contents which may be: (1) cyst epithe- plasma protein exudate & hyaluronic acid, products of epithelial
lium and its products of autolysis; (2) plasma proteins derived from cell breakdown together contribute to the high osmotic pressure of
transudation, exudation, and intracystic haemorrhage; (3) tissue the cystic fluid on cyst walls causing bone resorption by osteolysis,
fluid is drawn into the cyst owing to the high osmolality created and cyst enlargement.26
by (1) and (2); and (4) mucus secreted by the goblet cells which are Inflammatory Collateral Cyst possibly originates from either:
found in some follicular and nasopalatine cyst walls, either of these crevicular epithelium, the cell rests of Malassez and the reduced
create expansile force.13,14,15,16 The capsule, an essential supporting enamel epithelium. Craig explained the frequent buccal location
connective tissue matrix, is probably induced by the proliferating of the cyst is attributed due to the presence of an extension of
epithelium similarly to that described in tumours by Folkman. An reduced enamel epithelium over the enamel projections.27 Acker-
equally important consideration is the resorption of the surround- mann et al. (1987) suggested that cyst formation occurs as a result
ing bone.17,18,19,20 Humoral agents like parathyroid hormone, vitamin of the unilateral expansion of the dental follicle secondary to in-
D (I,25-dihydroxycholecalciferol), prostaglandins, and a lympho- flammatory destruction of periodontium and the alveolar bone.28
kine produced by stimulated B lymphocytes, the osteoclast-activat- Colgan et al. believe that the food impaction in the soft tissues oc-
ing factor activate the bone-resorbing cells.21,22,26 As the cyst grows cludes the opening of a pericoronal pocket, and as a consequence
in size, the periosteum is stimulated to form a layer of new bone, of inflammation the fluid accumulates within this obstructed pock-
and this deposition later involves the outline of the affected portion et by osmotic process leading to cystic expansion.29
of the jaw producing enlargement. Initially, the lateral expansion Dentigerous cyst results from inflammatory exudate pooling
causes smooth, hard, painless prominence. Bone covering the cen- between reduced enamel epithelium and crown of the tooth or be-
tre of the convexity is thinned with the cyst growth which can be tween the layers of the enamel epithelium itself. The exudate is de-
indented with pressure. In some cases, an area with no bone results rived from obstructed follicular veins of an unerupted tooth.16,21
in a window as the periosteum is unable to maintain the new bone In contrast to inflammatory cysts, no epithelial proliferation is
formation. This fragile outer shell of bone becomes fragmented and needed to form this cyst.22 The cyst wall is derived from the den-
the sensation imparted on palpation. Further distension of cyst wall tal follicle, made of scattered odontogenic epithelial rests which
can lead to a discharge of fluid into the mouth.23 sometimes exhibit dystrophic calcification. Mucus-producing cells,
Radicular Cyst arises from the proliferation of the epithelial rests as well as ciliated cells, may be observed in the lining, which marks
of Malassez (Harris and Toller 1975) in a focus of inflammation that the multipotentiality of the cells of the dental lamina. Cyst enlarges
has led to to the formation of a periapical granuloma. Hertwig’s epi- by unicentric expansion from the hydrostatic pressure of its con-
thelial root sheath remanants lying within this granuloma may in- tents. When secondarily inflammed this cystic epithelial lining be-
crease due to the inflammatory stimulus and through subsequent comes thick, forming rete ridges and densely collagenized.17 Rarely,
liquefaction necrosis in the centre of these enlarged epithelial nests, secondary development of neoplastic lesions like: Adenomatoid
a fluid-filled cyst with an epithelial lining forms.23 It enlarges by Odontogenic Tumour,  Complex Odontoma, Ameloblastoma, Mu-
unicentric expansion from the hydrostatic pressure of its contents. coepidermoid Carcinoma, and Squamous Cell Carcinoma have
Rarely, the epithelium may be derived from the maxillary sinus in been documented. Although the precise mechanism of malignant
cases of maxillary teeth that have extended into the sinus wall.24 Lin transformation in the lining epithelium remains unknown, long-
et al. explained how the epithelium-lined apical cyst is formed. As term chronic inflammation may stimulate this transformation.18 
epithelial islands expand, central epithelial cells are distanced from Odontogenic Keratocyst growth along the cancellous channels
with very little cortical expansion is explained in theories including:

32 Oral and Maxillofacial Pathology Journal, Volume 12 Issue 1 (January–June 2021)

intraluminal hyperosmolality, active epithelial proliferation30, the apoptotic Bcl-2 might be associated with deregulation of cell death
collagenolytic activity of the cyst wall31 and synthesis of interleu- in the lining epithelium, while Ki-67 and p53 role was insignificant
kin 1 and 6 by keratinocytes that tend to activate the resorption in cell proliferation.50, 51
of bone around the lesions by stimulating osteoclastogenesis.32,33 Calcifying Odontogenic Cyst is a unique lesion possessing both
de Paula A M et al. concluded that inflammation induces increase cystic and neoplastic potential. Praetorius argues that it is not just
epithelial cell proliferation which is associated with disruption of a developmental cyst as it often forms islands of epithelium and
the typical structure of cyst linings. Hirshberg A et al. stated that in- dentinoid in the wall; while in some an odontoma forms.52 The cells
flammation had an impact on collagen fibre packing in connective responsible for the cyst formation are rests of serres within the soft
tissue wall of cyst, as reflected by their birefringence under polar- tissue or bone. Therefore, these cysts are of primordial origin and
ized light.34 The expression levels of TGF-α, EGF and EGFR suggest are not associated with the crown of an impacted tooth. It most
the involvement of the growth factors in their pathogenesis.32 The often occurs as a central lesion, with peripheral localization being a
overexpression of p53 protein is related to the proliferative capacity rarity.53 McGowan and Browne, in 1982, found that the presence of
of this entity rather than increased numbers of p53+ cells.35,36 Ki- mineralization was approximately twice as frequent in microscopic
67 expression is higher in the epithelium when compared to other examination compared to radiographic analysis.54 Several epithe-
developmental and inflammatory cysts, with most of the Ki-67+ lial cells which are eosinophilic devoid of any nuclei, with their ba-
cells being detected in the suprabasal layers. sic cell outline retained named as ghost cells are seen which may
Lateral Periodontal Cyst (LPC) origin is debatable. Various re- undergo calcification and lose their cellular outline to form a firm
searchers provide support for the lesion developing from either sheet-like area, of calcified keratin.55,56 Ghost cells are thought to
dental lamina, reduced enamel epithelium or epithelial rests of be resulting from coagulative necrosis and dystrophic calcification,
Malassez.37 Inflammation does not play a role in their development. or a form of normal or abnormal keratinization of the odontogenic
The pathogenesis may be related to the 3 hypotheses: (1) Cyst is epithelium. The ability to induce dental hard tissue formation ap-
lined by nonkeratinized epithelium reminiscent of the reduced pears to be a property of epithelial cell lining of this cyst.
enamel epithelium which is supported by PCNA immunohisto- Orthokeratinized odontogenic cyst (OOC) pathogenesis is yet
chemical expression. (2) related to dental lamina remnants, as it to be unravelled.  According Thosaporn et al. it should always be
histopathologically presents glycogen-rich clear cells, which are considered in the differential diagnosis of radiolucent lesions in-
seen in the dental lamina aswell. (3) that the epithelial remnants of volving impacted teeth, in view of its origin from dental lamina.57
malassez presented in the roots surface, the central location of the CK7 and CK13, usually expressed by the dental lamina and enamel
cyst, play a role.38,39,40 The multilocular variant of Lateral Periodon- organ, are weakly positive in a dentigerous cyst, while OOC and OKC
tal cyst is “botryoid cyst”. Some consider it a result of changes in show the expression of only CK13. This supports the view that OKC
LPCs, others say it arises from fusion of multiple LPCs developing in and OOC may be derived from the dental lamina.58 Also, it is shown
proximity while most consider it arising from groups of converging that OOC expresses cytokeratins which are primarily expressed in
cellular debris of serres incorporated into the periodontal tissue, or epidermis, that explains the possibility of the sequestration of the
from the reduced enamel epithelium of the follicle which expands stomadial ectoderm into the developing jaw during embryogen-
to occupy a space in the periodontal ligament during the eruptive esis.59 The expression of Ki67, p53, p63 and BCL-2 were distinctly dif-
phase, where if a portion of this remains in the gum after the erup- ferent in OOC with reduced expression than OKC reflecting a lower
tion it forms a gingival cyst.42 Redman et al., stated that LPCs if left cellular activity and more indolent behaviour.60,61
untreated, may fuse to form a multicystic lesion referred as Botry-
oid variety.43 Van der Waal stated that Botryoid variety could not
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34 Oral and Maxillofacial Pathology Journal, Volume 12 Issue 1 (January–June 2021)

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