Immunohistochemical expression of SPARC in odontogenic keratocysts: a comparative study with other odontogenic cysts.

BACKGROUND: Secreted protein acidic and rich in cysteine (SPARC) has been shown to modulate aggressive behavior in several benign and malignant tumors. Little is known about SPARC expression in odontogenic keratocyst (OKC), an odontogenic cyst with an aggressive nature. To the best of our knowledge, only one study has been investigated the expression of this protein in OKCs. This study aimed to characterize SPARC expression in OKCs. Additionally, to determine whether SPARC is associated with aggressive behavior in OKCs, SPARC expression in OKCs was compared with radicular cysts (RCs), dentigerous cysts (DCs) and calcifying odontogenic cysts (COCs). These odontogenic cysts showed no or less aggressive behavior. METHODS: SPARC expression was evaluated in 38 OKCs, 39 RCs, 35 DCs and 14 COCs using immunohistochemistry. The percentages of positive cells and the intensities of immunostaining in the epithelial lining and the cystic wall were evaluated and scored. RESULTS: Generally, OKCs showed similar staining patterns to RCs, DCs and COCs. In the epithelial lining, SPARC was not detected, except for ghost cells in all COCs. In the cystic wall, the majority of positive cells were fibroblasts. Compared between 4 groups of odontogenic cysts, SPARC expression in OKCs was significantly higher than those of RCs (P < 0.001), DCs (P < 0.001) and COCs (P = 0.001). CONCLUSIONS: A significant increase of SPARC expression in OKCs compared with RCs, DCs and COCs suggests that SPARC may play a role in the aggressive behavior of OKCs.

Diagnostic potential of Type VII Collagen during oral carcinogenesis.

Type VII collagen (Col7) is a major component of anchoring fibrils. Col7 plays a role in tumor development and aggressiveness of cutaneous squamous cell carcinoma of recessive dystrophic epidermolysis bullosa. However, the role of Col7 in oral squamous cell carcinoma (OSCC) and oral leukoplakia (OL) remains largely unknown. To elucidate the role of Col7 and its diagnostic potential during oral carcinogenesis. Col7 expression was immunohistochemically studied in 254 samples, including normal oral mucosa (NM), OL without dysplasia, OL with dysplasia, and OSCC. The correlation between Col7 expression and clinicopathologic parameters of OSCC was also determined. Col7 was present as a linear deposit at the basement membrane of NM, OL without dysplasia and OL with dysplasia, and at the tumor-stromal junction around tumor islands in OSCC. Discontinuity of expression was frequently observed in OL with dysplasia and OSCC. OSCC had the significantly lowest Col7 expression (p<0.0001). Compared with OL without dysplasia, OL with dysplasia showed significantly reduced Col7 expression. Patients in clinical stage 4 with positive nodes had low Col7 expression compared with those in clinical stage 1 and negative nodes, respectively. Loss of Col7 is associated with tumorigenesis and aggressiveness in OSCC. A significantly reduced Col7 expression in OSCC implies that Col7 may be a useful marker for diagnosis and therapeutic targets.

Diagnostic potential of Type VII Collagen during oral carcinogenesis

Abstract Type VII collagen (Col7) is a major component of anchoring fibrils. Col7 plays a role in tumor development and aggressiveness of cutaneous squamous cell carcinoma of recessive dystrophic epidermolysis bullosa. However, the role of Col7 in oral squamous cell carcinoma (OSCC) and oral leukoplakia (OL) remains largely unknown. Objective To elucidate the role of Col7 and its diagnostic potential during oral carcinogenesis. Methodology Col7 expression was immunohistochemically studied in 254 samples, including normal oral mucosa (NM), OL without dysplasia, OL with dysplasia, and OSCC. The correlation between Col7 expression and clinicopathologic parameters of OSCC was also determined. Results Col7 was present as a linear deposit at the basement membrane of NM, OL without dysplasia and OL with dysplasia, and at the tumor-stromal junction around tumor islands in OSCC. Discontinuity of expression was frequently observed in OL with dysplasia and OSCC. OSCC had the significantly lowest Col7 expression (p<0.0001). Compared with OL without dysplasia, OL with dysplasia showed significantly reduced Col7 expression. Patients in clinical stage 4 with positive nodes had low Col7 expression compared with those in clinical stage 1 and negative nodes, respectively. Conclusion Loss of Col7 is associated with tumorigenesis and aggressiveness in OSCC. A significantly reduced Col7 expression in OSCC implies that Col7 may be a useful marker for diagnosis and therapeutic targets.

Epithelial and fibroblast SPARC expression patterns in oral leukoplakia and oral squamous cell carcinoma.

OBJECTIVE: This study evaluated and compared the expression of secreted protein acidic and rich in cysteine (SPARC) in epithelial cells and fibroblasts of oral leukoplakia (OL) and oral squamous cell carcinoma (OSCC) using normal oral mucosa as a control. STUDY DESIGN: The expression of SPARC was determined in samples of normal oral mucosa (n = 12), OL without dysplasia (n = 31), OL with dysplasia (n = 54), and OSCC (n = 69) using immunohistochemistry. The percentage of positive cells in epithelial cells and fibroblasts was independently evaluated. RESULTS: Epithelial SPARC was found in 33.3%, 35.5%, 25.9%, and 66.7% of normal oral mucosa, OL without dysplasia, OL with dysplasia, and OSCC, respectively. Fibroblast SPARC was found in 50.0%, 29.0%, 46.3%, and 84.1% of normal oral mucosa, OL without dysplasia, OL with dysplasia, and OSCC, respectively. OSCC had higher epithelial and fibroblast SPARC expression than normal oral mucosa, OL without dysplasia, and OL with dysplasia (P < .05). No significant differences were observed in epithelial and fibroblast SPARC among normal oral mucosa or OL with and without dysplasia. CONCLUSION: Overexpression of epithelial and fibroblast SPARC was observed in OSCC but not in OL, suggesting that SPARC is involved in the late stage of oral carcinogenesis.

Diagnostic Value of Cytokeratin 17 during Oral Carcinogenesis: An Immunohistochemical Study.

BACKGROUND: Little is known about the role of cytokeratin 17 (CK17) during oral carcinogenesis. CK17 expression in oral leukoplakia (OL), the most encountered oral potentially malignant disorders and oral squamous cell carcinoma (OSCC), remains very limited. To determine the role of CK17 during oral carcinogenesis and its potential diagnostic marker in oral premalignant and malignant lesions, this study evaluated CK17 expression in OL without dysplasia, OL with dysplasia, and OSCC. CK17 expression in these tissues was compared with those of normal oral mucosa (NOM). Additionally, the relationship between CK17 expression and clinicopathologic factors of OSCC was investigated. METHODS: CK17 expression was evaluated in 186 samples consisting of 12 NOM, 33 OL without dysplasia, 58 OL with dysplasia, and 83 OSCC using immunohistochemistry. The proportion of positively immunostained cells was evaluated and scored. RESULTS: CK17 was expressed in 8.3%, 54.5%, 74.1%, and 90.4% of NOM, OL without dysplasia, OL with dysplasia, and OSCC, respectively. NOM had a significantly lower CK17 score than OL with dysplasia (p=0.0003) and OSCC (p < 0.0001). A significant association between CK17 expression and histopathologic differentiation of OSCC was found. Tumors with well differentiation had high CK17 expression compared with those of moderate and poor differentiation. CONCLUSION: CK17 was overexpressed in OL with dysplasia and OSCC, suggesting that CK17 plays a pivotal role in the development of premalignant lesions and OSCC. Of clinical significance, CK17 may be a good diagnostic marker for oral premalignant lesions and OSCC. Additionally, CK17 could be used as an objective tool to classify histopathologic grade in OSCC. The findings that CK17 expression is high in OSCC but low in NOM imply that CK17 may serve as a potential therapeutic target for OSCC.

Non-endodontic periapical lesions clinically diagnosed as endodontic periapical lesions: A retrospective study over 15 years.

BACKGROUND: This study aimed to provide the frequency and demographic data of non-endodontic periapical lesions clinically misdiagnosed as endodontic periapical lesions from a Southeast Asian population over a 15-year period. MATERIAL AND METHODS: A retrospective study was conducted from departmental archives between 2005 and 2019. Cases clinically diagnosed as endodontic periapical lesions were retrieved. Then, cases with a histopathological diagnosis of non-endodontic periapical lesion were selected. Demographic data of non-endodontic periapical lesions were recorded. Radiographic features of cases with available radiographs were analyzed. RESULTS: Of 1,566 cases clinically diagnosed as endodontic periapical lesion, 157 cases received a histopathological diagnosis of non-endodontic origin. Eighteen different histopathological diagnoses were identified. The most frequent lesion was dentigerous cyst (n= 51, 32.48%) followed by odontogenic keratocyst (n=31, 19.75%), nasopalatine duct cyst (n=18, 11.46%) and ameloblastoma (n=15, 9.56%). Three cases of malignant tumors, including adenoid cystic carcinoma, mucoepidermoid carcinoma, and metastatic papillary thyroid carcinoma were observed. CONCLUSIONS: Non-endodontic periapical lesions constituted 10.03% of cases clinically diagnosed as endodontic periapical lesions. Histopathological examinations of non-endodontic periapical lesions revealed a variety of lesions ranging from foreign body reaction, cysts, fibro-osseous lesions, benign tumors and primary or metastatic malignant tumors. Of clinical significance is that some non-endodontic periapical lesions had different treatment modalities and prognoses compared with endodontic lesions. Therefore, dentists must be aware that periapical radiolucent lesions are not always a consequence of pulpal necrosis. Key words:Ameloblastoma, dentigerous cyst, endodontic periapical lesions, non-endodontic periapical lesions, odontogenic keratocyst.

Intraoral Oncocytic Mucoepidermoid Carcinoma - A Rare Case Report and Review of the Literature.

Rationale: Oncocytic mucoepidermoid carcinoma (OMEC) is a rare variant of mucoepidermoid carcinoma (MEC). The parotid gland is the most common site of OMEC, whereas intraoral OMEC is infrequent. Patient Concerns: A 55-year-old male presented with an asymptomatic mass at the palate for 20 years. Diagnosis: Incisional biopsy showed classic MEC. Treatment: The patient underwent partial maxillectomy under general anaesthesia. The excised specimen revealed sheets of oncocytes additional to the tumour cells found in the incisional biopsy. Additional special stain and immunohistochemical stain confirmed the diagnosis of OMEC. Outcomes: The patient was followed up for 3 years with no recurrence. Take-away Lessons: The diagnosis of OMEC needs to be differentiated from other salivary gland tumours containing oncocytes. Moreover, the conventional grading system applied to OMEC may not correlate with their behavior and may need further review.

Ameloblastic carcinoma ex ameloblastoma of the maxilla.

Ameloblastic carcinoma (AC) is a rare malignant odontogenic tumor. Approximately 138 cases were reported. The majority of these cases occurred in the mandible. Only 57 cases were located in the maxilla. Most of AC cases occur in a primary type. Little is known about AC secondary type (dedifferentiated) since only six cases have been reported. All of previous six cases occurred in the mandible. Here, we presented the first case of maxillary AC secondary type (dedifferentiated) in a 46-year-old female. The first excisional biopsy was diagnosed as basal cell ameloblastoma. Then, the patient underwent partial maxillectomy. A recurrence occurred 17 months later. At this time, tumor cells with cytological atypia were clearly detected. A diagnosis of AC was rendered. Two years later, the patient suffered from another recurrence and received a wide excision with a diagnosis of AC. We considered our case as AC secondary type (dedifferentiated). We discussed the histopathological findings that may be helpful in making a diagnosis of AC. In addition, we consider that the basaloid pattern may be related to malignant transformation in ameloblastoma.