Glandular odontogenic cyst

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Template:Short description Template:Infobox medical condition

A glandular odontogenic cyst (GOC) is a rare and usually benign odontogenic cyst developed at the odontogenic epithelium of the mandible or maxilla.[1][2][3][4] Originally, the cyst was labeled as "sialo-odontogenic cyst" in 1987.[5] However, the World Health Organization (WHO) decided to adopt the medical expression "glandular odontogenic cyst".[3] Following the initial classification, only 60 medically documented cases were present in the population by 2003.[6] GOC was established as its own biological growth after differentiation from other jaw cysts such as the "central mucoepidermoid carcinoma (MEC)", a popular type of neoplasm at the salivary glands.[5][7] GOC is usually misdiagnosed with other lesions developed at the glandular and salivary gland due to the shared clinical signs.[8] The presence of osteodentin supports the concept of an odontogenic pathway.[4] This odontogenic cyst is commonly described to be a slow and aggressive development.[9] The inclination of GOC to be large and multilocular is associated with a greater chance of remission.[4][10] GOC is an infrequent manifestation with a 0.2% diagnosis in jaw lesion cases.[11] Reported cases show that GOC mainly impacts the mandible and male individuals.[10] The presentation of GOC at the maxilla has a very low rate of incidence.[2] The GOC development is more common in adults in their fifth and sixth decades.[12]

GOC has signs and symptoms of varying sensitivities, and dysfunction.[9][11] In some cases, the GOC will present no classic abnormalities and remains undiagnosed until secondary complications arise.[9] The proliferation of GOC requires insight into the foundations of its unique histochemistry and biology.[5] The comparable characteristics of GOC with other jaw lesions require the close examination of its histology, morphology, and immunocytochemistry for a differential diagnosis.[4] Treatment modes of the GOC follow a case-by-case approach due to the variable nature of the cyst.[13] The selected treatment must be accompanied with an appropriate pre and post-operative plan.[13]

Signs and Symptoms

The appearance of a protrusive growth will be present at their mandible or maxilla.[1] The expansive nature of this cyst may destruct the quality of symmetry at the facial region and would be a clear physical sign of abnormality.[1][5] The area of impact may likely be at the anterior region of mandible as described in a significant number of reported cases.[2] At this region, GOC would eventually mediate expansion at the molars.[5] A painful and swollen sensation at the jaw region caused by GOC may be reported.[11] Detailing of a painless feeling or facial paraesthesia can be experienced.[5][11] Alongside GOC, "root resorption, cortical bone thinning and perforation, and tooth displacement may occur".[10] Experience of swelling at the buccal and lingual zones can occur.[6] Usually, the smaller sized GOCs present no classical signs or symptoms to the case (i.e. "asymptomatic").[14] GOC is filled with cystic a fluid that differs in viscosity and may appear as transparent, brownish-red, or creamy in colour.[10]

Causes

File:PDB 1ysw EBI.jpg
The molecular arrangement of BCL-2 protein, a potential cause to the development of the GOC. The protein can inhibit the process of apoptosis when at a high abundance.

The GOC can arise through a number of causes:[5]

The origin of the GOC can be understood through its biological and histochemistry foundations.[14] It has been suggested that GOC can be a result of a traumatic event.[8] The occurrence of GOC may be from a mutated cell from "the oral mucosa and the dental follicle" origin.[15] Another probable cause is from pre-existing cysts or cancerous constituents.[8] A potential biological origin of GOC is a cyst developed at a salivary gland or simple epithelium, which undergoes maturation at the glandular.[14] Another origin is a primordial cyst that infiltrates the glandular epithelial tissue through a highly organised cellular differentiation.[14] Pathologists discovered a BCL-2 protein, commonly present in neoplasms, to exist in the tissue layers of the GOC.[14][15] The protein is capable of disrupting normal cell death function at the odontogenic region.[14][15] The analysis of PTCH, a gene that specialises in neoplasm inhibition, was carried out to determine if any existing mutations played a role in the initiation of the GOC.[5] It is confirmed that the gene had no assistance in triggering cystic advancement.[5]

Diagnosis

Radiology

The performance of radiographic imaging i.e. computed tomography, at the affected area is considered essential.[9] Radiographic imaging of the GOC can display a defined unilocular or multilocular appearance that may be "rounded or oval" shaped upon clinical observation.[13][14] Scans may present a distribution of the GOC at the upper jaw as it presents a 71.8% prevalence in cases.[1] The margin surrounding the GOC is usually occupied with a scalloped definition.[1] A bilateral presentation of the GOC is possible but is not common at either the maxilla or mandible sites.[9] The GOC has an average size of 4.9 cm that can develop over the midline when positioned at the mandible or maxilla region.[10][11] Analysis of scans allow for the differentiation of GOC from other parallel lesions, i.e. "ameloblastoma, odontogenic myxoma, or dentigerous cyst" in order to minimise the chance of a misdiagnosis.[13] These scans can display the severity of cortical plate, root, and tooth complications, which is observed to determine the necessary action for reconstruction.[13]

Histology

Histological features related to the GOC differ in each scenario; however, there is a general criterion to identify the cyst.[11] The GOC usually features a "stratified squamous epithelium" attached to connective tissue that is filled with active immune cells.[1][5] The lining of the epithelium features a very small diameter that is usually non-keratinised.[2][9] In contrast, the lining of the GOC has rather an inconsistent diameter.[1] The basal cells of the GOC usually has no association to a cancerous origin.[8] Tissue cells can be faced with an abnormal increase in the concentration of calcium, which can cause the region to calcify.[5] The transformation of the epithelium is associated with a focal luminal development.[1] Eosinophilic organelles such as columnar and cuboidal cells can be observed during microscopy.[7] Intra-epithelial crypts may be identified in the internal framework of the epithelium or at the external space where it presents itself as papillae protrusions.[2][9] Mucin is observable after the application of "alcian blue dye" on the tissue specimen.[2] The histological observation of goblet cells is a common feature with the "odontogenic dentigerous cyst".[7] In some circumstances, the epithelium can have variable plaque structures that appear as swirls in the tissue layers.[2] Interestingly, histologists were able to identify hyaline bodies within the tissue framework of the GOC.[5] It is encouraged that the histological identification of at least seven of these biological characteristics is required to accurately distinguish the presence of the GOC.[7]

Intraepithelial Hemosiderin

Pathologists have identified hemosiderin pigments that are considered unique to the GOC.[8] The discovery of this pigment can be pivotal to the differentiation of the GOC from other lesions.[8] The staining at the epithelium is due to the haemorrhaging of the lining.[8] The cause of the haemorrhaging can be triggered by the type of treatment, cellular degradation, or structural deformation inflicted during GOC expansion.[8] Examination of the GOC tissue section indicated that red blood cells from the intraluminal space had combined with the extracellular constituents.[8] This process is carried out through transepithelial elimination.[8] This clinical procedure is beneficial to confirm the benign or malignant nature of the GOC.[8]

Immunocytochemistry

The examination of cytokeratin profiles is deemed useful when observing the differences between the GOC and the central MEC.[11] These two lesions show individualised expression for cytokeratin 18 and 19.[5] Past studies observed Ki-67, p53, and PCNA expression in common jaw cysts that shared similar characteristics.[5] There was a lack of p53 expression found in radicular cysts.[5] Similarly, Ki-67 was seen less in the central MEC compared to the other lesions, though this discovery is not essential to the process of differential diagnosis.[5][11] Proliferating cell nuclear antigen readings were established to have no role in the differentiation process.[11] The TGF-beta marker is present in the GOC and can explain the limited concentration of normal functioning cells.[15]

MAML2 rearrangement

The observation of a MAML2 rearrangement is described as a procedure useful in the differential diagnosis of the GOC and its closely related lesion, the central MEC.[7] A second cystic development displayed the presence of CRTC3-MAML2 fusion after an in-vitro application.[7] The MAML2 rearrangement represents the developmental growth of the central MEC from the GOC.[7] The use of fusion-gene transcript may be helpful towards the differentiation of the GOC from the central MEC of the jaw and salivary glands.[7]

Treatment

Pre-treatment protocols

File:Panoramic Xray.jpg
Panoramic radiography used to provide visualisations of the maxilla and mandible. X-rays will display the degree of impact on case, caused by the GOC.

A computed tomography and panoramic x-ray must be undertaken in order to observe the severity of internal complications.[13] These scans allow for the observation of the GOC size, radiolucency, cortical bone, dentition, root, and vestibular zone.[13] In some cases, the dentition may be embedded into the cavity walls of the lesion, depending on the position of expansion at the odontogenic tissue.[9] The diagnosis of a smaller sized GOC is related to the attachment of only two teeth.[6] While, a greater sized GOC develops over two teeth.[6] Presentation of a greater sized lesion usually requires a biopsy for a differential diagnosis and a precise treatment plan.[6]

Treatment process

The unilocular and multilocular nature is imperative to the determination of treatment style.[6] Local anesthesia is regularly provided as the GOC is embedded within the tissue structure of the jaw and requires an invasive procedure for a safe and accurate extraction.[1] For unilocular GOCs with minimal tissue deterioration, "enucleation, curettage, and marsupialization" is a suitable treatment plan.[6] Notably, the performance of enucleation or curettage as the primary action is linked to an incomplete extraction of the GOC and is only recommended to the less invasive lesions.[6] Multilocular GOCs require a more invasive procedure such as "peripheral ostectomy, marginal resection, or partial jaw resection".[6] GOCs associated with a more severe structural damage are encouraged to undergo marsupialization as either an initial or supplementary surgery.[6] The frequency of reappearance is likely due to the lingering cystic tissue structures that remain after the performance of curettage.[9] The incorporation of a "dredging method i.e. repetition of enucleation and curettage" is also suggested until the remnants of the GOC diminishes for certain.[3] The treatment ensures scar tissue is removed to promote the successful reconstruction of osseous material for jaw preservation.[3] Alongside the main treatments, bone allograft application, cryosurgery, and apicoectomy are available but have not been consistently recommended.[3][9][13] Though Carnoy's solution, the chloroform-free version, is recommended with the treatment as it degenerates the majority of the damaged dental lamina.[9] The most effective type of treatment remains unknown due to the lack of detailed data from reported cases.[10]

Post-treatment protocols

Follow-up appointments are necessary after the removal of the GOC as there is a high chance of remission, which may be exacerbated in cases dealing with "cortical plate perforation".[9][13] The GOC has a significant remission rate of 21 to 55% that can potentially develop during the period of 0.5 to 7 years post-surgery.[5][6] Cases occupied with a lower risk lesion are expected to continue appointments with physicians for up to 3 years post-surgery.[6] A higher risk lesion is encouraged to consistently consult with physicians during a 7-year period after treatment.[9] Remission events require immediate attention and appropriate procedures such as enucleation or curettage.[6] In more damaging cases of remission, tissue resection, and marsupialization may have to be performed.[5]

Epidemiology

The clinical presentation of the GOC is very low in the population as noted by the 0.12 to 0.13% occurrence rate, extrapolated from a sample size of the 181 individuals.[1] The GOC mainly affects older individuals in the population, especially those that are in their 40 to 60s.[2] However, the GOC can affect younger individuals i.e. 11, and more older individuals i.e. 82 in the population.[1] The age distribution starts at a much lower number for people living in Asia and Africa.[1] Those in their first 10 years of life have not been diagnosed with the GOC.[11] The GOC does present a tendency to proliferate in more males than females.[10] There is no definitive conclusion towards the relevance of gender and its influence on the rate of incidence.[5]

References

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Bibliography

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Further reading

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