Glandular odontogenic cyst | |
---|---|
Other names | Sialo-Odontogenic cyst |
![]() | |
Relative incidence of odontogenic cysts. [1] Glandular odontogenic cyst is labeled at bottom. | |
Symptoms | Jaw expansion, swelling, impairment to the tooth, root and cortical plate [2] [3] |
Causes | Cellular mutation, cyst maturation at glandular, BCL-2 protein [2] [4] |
Diagnostic method | Biopsy, CT scans, Panoramic x-rays [5] [6] |
Differential diagnosis | Central mucoepidermoid carcinoma, odontogenic keratocyst [7] [6] |
Prevention | Post-surgery follow-ups are commonly proposed to prevent the chances of recurrence [6] |
Treatment | Enucleation, curettage, marginal or partial resection, marsupialization [6] |
Frequency | 0.12 to 0.13% of people [2] |
A glandular odontogenic cyst (GOC) is a rare and usually benign odontogenic cyst developed at the odontogenic epithelium of the mandible or maxilla. [2] [8] [9] [10] Originally, the cyst was labeled as "sialo-odontogenic cyst" in 1987. [7] However, the World Health Organization (WHO) decided to adopt the medical expression "glandular odontogenic cyst". [9] 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. [7] [11] GOC is usually misdiagnosed with other lesions developed at the glandular and salivary gland due to the shared clinical signs. [12] The presence of osteodentin supports the concept of an odontogenic pathway. [10] This odontogenic cyst is commonly described to be a slow and aggressive development. [13] The inclination of GOC to be large and multilocular is associated with a greater chance of remission. [10] [3] GOC is an infrequent manifestation with a 0.2% diagnosis in jaw lesion cases. [14] Reported cases show that GOC mainly impacts the mandible and male individuals. [3] The presentation of GOC at the maxilla has a very low rate of incidence. [8] The GOC development is more common in adults in their fifth and sixth decades. [1]
GOC has signs and symptoms of varying sensitivities, and dysfunction. [13] [14] In some cases, the GOC will present no classic abnormalities and remains undiagnosed until secondary complications arise. [13] The proliferation of GOC requires insight into the foundations of its unique histochemistry and biology. [7] The comparable characteristics of GOC with other jaw lesions require the close examination of its histology, morphology, and immunocytochemistry for a differential diagnosis. [10] Treatment modes of the GOC follow a case-by-case approach due to the variable nature of the cyst. [5] The selected treatment must be accompanied with an appropriate pre and post-operative plan. [5]
The appearance of a protrusive growth will be present at their mandible or maxilla. [2] 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. [2] [7] The area of impact may likely be at the anterior region of mandible as described in a significant number of reported cases. [8] At this region, GOC would eventually mediate expansion at the molars. [7] A painful and swollen sensation at the jaw region caused by GOC may be reported. [14] Detailing of a painless feeling or facial paraesthesia can be experienced. [7] [14] Alongside GOC, " root resorption, cortical bone thinning and perforation, and tooth displacement may occur". [3] 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"). [4] GOC is filled with cystic a fluid that differs in viscosity and may appear as transparent, brownish-red, or creamy in colour. [3]
The GOC can arise through a number of causes: [7]
The origin of the GOC can be understood through its biological and histochemistry foundations. [4] It has been suggested that GOC can be a result of a traumatic event. [12] 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. [12] A potential biological origin of GOC is a cyst developed at a salivary gland or simple epithelium, which undergoes maturation at the glandular. [4] Another origin is a primordial cyst that infiltrates the glandular epithelial tissue through a highly organised cellular differentiation. [4] Pathologists discovered a BCL-2 protein, commonly present in neoplasms, to exist in the tissue layers of the GOC. [4] [15] The protein is capable of disrupting normal cell death function at the odontogenic region. [4] [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. [7] It is confirmed that the gene had no assistance in triggering cystic advancement. [7]
The performance of radiographic imaging i.e. computed tomography, at the affected area is considered essential. [13] Radiographic imaging of the GOC can display a defined unilocular or multilocular appearance that may be "rounded or oval" shaped upon clinical observation. [5] [4] Scans may present a distribution of the GOC at the upper jaw as it presents a 71.8% prevalence in cases. [2] The margin surrounding the GOC is usually occupied with a scalloped definition. [2] A bilateral presentation of the GOC is possible but is not common at either the maxilla or mandible sites. [13] The GOC has an average size of 4.9 cm that can develop over the midline when positioned at the mandible or maxilla region. [3] [14] 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. [5] These scans can display the severity of cortical plate, root, and tooth complications, which is observed to determine the necessary action for reconstruction. [5]
Histological features related to the GOC differ in each scenario; however, there is a general criterion to identify the cyst. [14] The GOC usually features a " stratified squamous epithelium" attached to connective tissue that is filled with active immune cells. [2] [7] The lining of the epithelium features a very small diameter that is usually non-keratinised. [8] [13] In contrast, the lining of the GOC has rather an inconsistent diameter. [2] The basal cells of the GOC usually has no association to a cancerous origin. [12] Tissue cells can be faced with an abnormal increase in the concentration of calcium, which can cause the region to calcify. [7] The transformation of the epithelium is associated with a focal luminal development. [2] Eosinophilic organelles such as columnar and cuboidal cells can be observed during microscopy. [11] 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. [8] [13] Mucin is observable after the application of " alcian blue dye" on the tissue specimen. [8] The histological observation of goblet cells is a common feature with the "odontogenic dentigerous cyst". [11] In some circumstances, the epithelium can have variable plaque structures that appear as swirls in the tissue layers. [8] Interestingly, histologists were able to identify hyaline bodies within the tissue framework of the GOC. [7] 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. [11]
Pathologists have identified hemosiderin pigments that are considered unique to the GOC. [12] The discovery of this pigment can be pivotal to the differentiation of the GOC from other lesions. [12] The staining at the epithelium is due to the haemorrhaging of the lining. [12] The cause of the haemorrhaging can be triggered by the type of treatment, cellular degradation, or structural deformation inflicted during GOC expansion. [12] Examination of the GOC tissue section indicated that red blood cells from the intraluminal space had combined with the extracellular constituents. [12] This process is carried out through transepithelial elimination. [12] This clinical procedure is beneficial to confirm the benign or malignant nature of the GOC. [12]
The examination of cytokeratin profiles is deemed useful when observing the differences between the GOC and the central MEC. [14] These two lesions show individualised expression for cytokeratin 18 and 19. [7] Past studies observed Ki-67, p53, and PCNA expression in common jaw cysts that shared similar characteristics. [7] There was a lack of p53 expression found in radicular cysts. [7] 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. [7] [14] Proliferating cell nuclear antigen readings were established to have no role in the differentiation process. [14] The TGF-beta marker is present in the GOC and can explain the limited concentration of normal functioning cells. [15]
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. [11] A second cystic development displayed the presence of CRTC3-MAML2 fusion after an in-vitro application. [11] The MAML2 rearrangement represents the developmental growth of the central MEC from the GOC. [11] 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. [11]
A computed tomography and panoramic x-ray must be undertaken in order to observe the severity of internal complications. [5] These scans allow for the observation of the GOC size, radiolucency, cortical bone, dentition, root, and vestibular zone. [5] 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. [13] 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]
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. [2] 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. [13] 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. [9] The treatment ensures scar tissue is removed to promote the successful reconstruction of osseous material for jaw preservation. [9] Alongside the main treatments, bone allograft application, cryosurgery, and apicoectomy are available but have not been consistently recommended. [9] [13] [5] Though Carnoy's solution, the chloroform-free version, is recommended with the treatment as it degenerates the majority of the damaged dental lamina. [13] The most effective type of treatment remains unknown due to the lack of detailed data from reported cases. [3]
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". [13] [5] 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. [7] [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. [13] 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. [7]
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. [2] The GOC mainly affects older individuals in the population, especially those that are in their 40 to 60s. [8] However, the GOC can affect younger individuals i.e. 11, and more older individuals i.e. 82 in the population. [2] The age distribution starts at a much lower number for people living in Asia and Africa. [2] Those in their first 10 years of life have not been diagnosed with the GOC. [14] The GOC does present a tendency to proliferate in more males than females. [3] There is no definitive conclusion towards the relevance of gender and its influence on the rate of incidence. [7]
Glandular odontogenic cyst | |
---|---|
Other names | Sialo-Odontogenic cyst |
![]() | |
Relative incidence of odontogenic cysts. [1] Glandular odontogenic cyst is labeled at bottom. | |
Symptoms | Jaw expansion, swelling, impairment to the tooth, root and cortical plate [2] [3] |
Causes | Cellular mutation, cyst maturation at glandular, BCL-2 protein [2] [4] |
Diagnostic method | Biopsy, CT scans, Panoramic x-rays [5] [6] |
Differential diagnosis | Central mucoepidermoid carcinoma, odontogenic keratocyst [7] [6] |
Prevention | Post-surgery follow-ups are commonly proposed to prevent the chances of recurrence [6] |
Treatment | Enucleation, curettage, marginal or partial resection, marsupialization [6] |
Frequency | 0.12 to 0.13% of people [2] |
A glandular odontogenic cyst (GOC) is a rare and usually benign odontogenic cyst developed at the odontogenic epithelium of the mandible or maxilla. [2] [8] [9] [10] Originally, the cyst was labeled as "sialo-odontogenic cyst" in 1987. [7] However, the World Health Organization (WHO) decided to adopt the medical expression "glandular odontogenic cyst". [9] 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. [7] [11] GOC is usually misdiagnosed with other lesions developed at the glandular and salivary gland due to the shared clinical signs. [12] The presence of osteodentin supports the concept of an odontogenic pathway. [10] This odontogenic cyst is commonly described to be a slow and aggressive development. [13] The inclination of GOC to be large and multilocular is associated with a greater chance of remission. [10] [3] GOC is an infrequent manifestation with a 0.2% diagnosis in jaw lesion cases. [14] Reported cases show that GOC mainly impacts the mandible and male individuals. [3] The presentation of GOC at the maxilla has a very low rate of incidence. [8] The GOC development is more common in adults in their fifth and sixth decades. [1]
GOC has signs and symptoms of varying sensitivities, and dysfunction. [13] [14] In some cases, the GOC will present no classic abnormalities and remains undiagnosed until secondary complications arise. [13] The proliferation of GOC requires insight into the foundations of its unique histochemistry and biology. [7] The comparable characteristics of GOC with other jaw lesions require the close examination of its histology, morphology, and immunocytochemistry for a differential diagnosis. [10] Treatment modes of the GOC follow a case-by-case approach due to the variable nature of the cyst. [5] The selected treatment must be accompanied with an appropriate pre and post-operative plan. [5]
The appearance of a protrusive growth will be present at their mandible or maxilla. [2] 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. [2] [7] The area of impact may likely be at the anterior region of mandible as described in a significant number of reported cases. [8] At this region, GOC would eventually mediate expansion at the molars. [7] A painful and swollen sensation at the jaw region caused by GOC may be reported. [14] Detailing of a painless feeling or facial paraesthesia can be experienced. [7] [14] Alongside GOC, " root resorption, cortical bone thinning and perforation, and tooth displacement may occur". [3] 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"). [4] GOC is filled with cystic a fluid that differs in viscosity and may appear as transparent, brownish-red, or creamy in colour. [3]
The GOC can arise through a number of causes: [7]
The origin of the GOC can be understood through its biological and histochemistry foundations. [4] It has been suggested that GOC can be a result of a traumatic event. [12] 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. [12] A potential biological origin of GOC is a cyst developed at a salivary gland or simple epithelium, which undergoes maturation at the glandular. [4] Another origin is a primordial cyst that infiltrates the glandular epithelial tissue through a highly organised cellular differentiation. [4] Pathologists discovered a BCL-2 protein, commonly present in neoplasms, to exist in the tissue layers of the GOC. [4] [15] The protein is capable of disrupting normal cell death function at the odontogenic region. [4] [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. [7] It is confirmed that the gene had no assistance in triggering cystic advancement. [7]
The performance of radiographic imaging i.e. computed tomography, at the affected area is considered essential. [13] Radiographic imaging of the GOC can display a defined unilocular or multilocular appearance that may be "rounded or oval" shaped upon clinical observation. [5] [4] Scans may present a distribution of the GOC at the upper jaw as it presents a 71.8% prevalence in cases. [2] The margin surrounding the GOC is usually occupied with a scalloped definition. [2] A bilateral presentation of the GOC is possible but is not common at either the maxilla or mandible sites. [13] The GOC has an average size of 4.9 cm that can develop over the midline when positioned at the mandible or maxilla region. [3] [14] 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. [5] These scans can display the severity of cortical plate, root, and tooth complications, which is observed to determine the necessary action for reconstruction. [5]
Histological features related to the GOC differ in each scenario; however, there is a general criterion to identify the cyst. [14] The GOC usually features a " stratified squamous epithelium" attached to connective tissue that is filled with active immune cells. [2] [7] The lining of the epithelium features a very small diameter that is usually non-keratinised. [8] [13] In contrast, the lining of the GOC has rather an inconsistent diameter. [2] The basal cells of the GOC usually has no association to a cancerous origin. [12] Tissue cells can be faced with an abnormal increase in the concentration of calcium, which can cause the region to calcify. [7] The transformation of the epithelium is associated with a focal luminal development. [2] Eosinophilic organelles such as columnar and cuboidal cells can be observed during microscopy. [11] 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. [8] [13] Mucin is observable after the application of " alcian blue dye" on the tissue specimen. [8] The histological observation of goblet cells is a common feature with the "odontogenic dentigerous cyst". [11] In some circumstances, the epithelium can have variable plaque structures that appear as swirls in the tissue layers. [8] Interestingly, histologists were able to identify hyaline bodies within the tissue framework of the GOC. [7] 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. [11]
Pathologists have identified hemosiderin pigments that are considered unique to the GOC. [12] The discovery of this pigment can be pivotal to the differentiation of the GOC from other lesions. [12] The staining at the epithelium is due to the haemorrhaging of the lining. [12] The cause of the haemorrhaging can be triggered by the type of treatment, cellular degradation, or structural deformation inflicted during GOC expansion. [12] Examination of the GOC tissue section indicated that red blood cells from the intraluminal space had combined with the extracellular constituents. [12] This process is carried out through transepithelial elimination. [12] This clinical procedure is beneficial to confirm the benign or malignant nature of the GOC. [12]
The examination of cytokeratin profiles is deemed useful when observing the differences between the GOC and the central MEC. [14] These two lesions show individualised expression for cytokeratin 18 and 19. [7] Past studies observed Ki-67, p53, and PCNA expression in common jaw cysts that shared similar characteristics. [7] There was a lack of p53 expression found in radicular cysts. [7] 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. [7] [14] Proliferating cell nuclear antigen readings were established to have no role in the differentiation process. [14] The TGF-beta marker is present in the GOC and can explain the limited concentration of normal functioning cells. [15]
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. [11] A second cystic development displayed the presence of CRTC3-MAML2 fusion after an in-vitro application. [11] The MAML2 rearrangement represents the developmental growth of the central MEC from the GOC. [11] 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. [11]
A computed tomography and panoramic x-ray must be undertaken in order to observe the severity of internal complications. [5] These scans allow for the observation of the GOC size, radiolucency, cortical bone, dentition, root, and vestibular zone. [5] 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. [13] 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]
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. [2] 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. [13] 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. [9] The treatment ensures scar tissue is removed to promote the successful reconstruction of osseous material for jaw preservation. [9] Alongside the main treatments, bone allograft application, cryosurgery, and apicoectomy are available but have not been consistently recommended. [9] [13] [5] Though Carnoy's solution, the chloroform-free version, is recommended with the treatment as it degenerates the majority of the damaged dental lamina. [13] The most effective type of treatment remains unknown due to the lack of detailed data from reported cases. [3]
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". [13] [5] 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. [7] [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. [13] 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. [7]
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. [2] The GOC mainly affects older individuals in the population, especially those that are in their 40 to 60s. [8] However, the GOC can affect younger individuals i.e. 11, and more older individuals i.e. 82 in the population. [2] The age distribution starts at a much lower number for people living in Asia and Africa. [2] Those in their first 10 years of life have not been diagnosed with the GOC. [14] The GOC does present a tendency to proliferate in more males than females. [3] There is no definitive conclusion towards the relevance of gender and its influence on the rate of incidence. [7]