Calcifying Odontogenic Cyst Demonstrates Recurrent WNT Pathway Mutations and So-Called Adenoid Ameloblastoma-like Histology: Evidence Supporting Its Classification as a Neoplasm.

Calcifying odontogenic cyst (COC), once called calcifying cystic odontogenic tumor (CCOT), is classified under the category of odontogenic cysts. However, the proliferative capacity of the lesional epithelium and consistent nuclear ß-catenin expression raise questions about its current classification. This study aimed to determine whether COC would be better classified as a neoplasm in the histologic and molecular context. Eleven odontogenic lesions diagnosed as COC or CCOT were included in this study. The growth patterns of the lesional epithelium were analyzed histologically in all cases. ß-catenin immunohistochemistry and molecular profiling using Sanger sequencing and whole-exome sequencing were performed in 10 cases. Of the 11 cases studied, histologic features reminiscent of so-called adenoid ameloblastoma were observed in 72.7% (8/11), and small islands of clear cells extended into the wall in 36.4% (4/11). Intraluminal and/or mural epithelial proliferation was found in 72.7% of the cases (8/11). Nuclear ß-catenin expression was observed focally in all 10 cases studied, mainly highlighting epithelial cells forming morules and adjacent to dentinoid. CTNNB1 hotspot mutations were detected in 60.0% of the cases (6/10). All the remaining cases had frameshift mutations in tumor suppressor genes involved in the WNT pathway, including APC and NEDD4L. Recurrent WNT pathway mutations leading to nuclear translocation of ß-catenin and distinct epithelial growth patterns found in COC are the neoplastic features shared by its solid counterpart, dentinogenic ghost cell tumor, supporting its classification as a tumor rather than a cyst.

Tumor immune microenvironment in odontogenic carcinomas: Evaluation of the therapeutic potential of immune checkpoint blockade.

BACKGROUND: Despite recent advances in the use of immune checkpoint blockade (ICB) across various cancer types, its efficacy in odontogenic carcinomas remains unexplored. This study aims to investigate PD-L1 expression and the tumor immune microenvironment (TIME) in odontogenic carcinomas to determine the therapeutic potential of ICB and the significance of immune markers. METHODS: The expressions of PD-L1 and T cell markers (CD3, CD8, and FOXP3) were visualized by immunohistochemistry in 21 tissue samples of odontogenic carcinomas. Tumoral PD-L1 expression and the density and spatial distribution of T cell subsets were evaluated, from which TIME was determined. The associations of the variables with clinicopathological and prognostic factors were statistically analyzed. RESULTS: PD-L1 was positively expressed in 52.4% (11/21) of the cases studied. Among tumor types, ameloblastic carcinoma showed significantly higher PD-L1 expression (p = 0.016). TIME based on the intratumoral and stromal T cell distribution was immune-inflamed in 61.9% (13/21) and immune-excluded in 38.1% (8/21), with no immune-desert cases. PD-L1 expression was associated with the densities of all intratumoral T cell subsets (p = 0.03 for CD3, p = 0.03 for CD8, and p = 0.008 for FOXP3) but not with those of stromal T cells. High PD-L1 expression was associated with larger tumor size (p = 0.021), while the intratumoral CD8/CD3 ratio was inversely correlated with tumor size (p = 0.048). CONCLUSION: These findings indicate the involvement of adaptive immune resistance in a subset of odontogenic carcinomas and support the therapeutic potential of ICB in patients with these rare malignancies.

Sialadenoma papilliferum-like intraductal papillary tumour: an emerging entity with intercalated duct differentiation showing MAPK pathway activation in both ductal and myoepithelial cells.

Sialadenoma papilliferum-like intraductal papillary tumour (SP-IPT) is a recently described salivary gland tumour that shows identical morphology to sialadenoma papilliferum (SP) except for the lack of an exophytic papillary component. However, the immunohistochemical phenotypes and molecular profiles of SP-IPT remain unclear. This study aims to report new cases of SP-IPT and to determine its cellular differentiation and molecular basis. After histopathological review, four cases of SP-IPT were retrieved. Immunohistochemical staining was performed to analyse the expression patterns of cytokeratin 7 (CK7), p63, smooth muscle actin (SMA), vimentin, S100, mammaglobin, androgen receptor, SOX10, BRAF V600E-mutated protein, and phosphorylated ERK. Sanger sequencing was performed to determine the mutation status of the BRAF, KRAS, NRAS, and HRAS genes. All four cases affected the posterior mandible with a mean age of 62 years and a male-to-female ratio of 3:1. Histologically, all cases consisted of multiple tubular and cystic structures with varying sizes and shapes. The tubulocystic components were lined by a double or few-layered epithelium frequently showing a micropapillary pattern. The outer layer consisted of a rim of myoepithelial cells, which were CK7+/p63+/SMA+/vimentin+/S100+/SOX10+. The inner ductal cells were CK7+/S100+/SOX10+, consistent with intercalated duct differentiation. All cases harboured BRAF V600E mutations, but no other mutations were detected. The BRAF V600E-mutated protein and phosphorylated ERK were expressed in both ductal and myoepithelial cells. These findings demonstrate the immunohistochemical and molecular similarities between SP-IPT and SP and the role and extent of MAPK pathway activation in the pathogenesis of SP-IPT.

Neuropilin-2 acts a critical determinant for epithelial-to-mesenchymal transition and aggressive behaviors of human head and neck cancer.

PURPOSE: Neuropilin-2 (NRP2) is a multifunctional single-pass transmembrane receptor that binds to two disparate ligands, namely, vascular endothelial growth factors (VEGFs) and semaphorins (SEMAs). It is reportedly involved in neuronal and vascular development. In this study, we uncovered the exact functional role of NRP2 and its molecular mechanism during aggressive behaviors and lymph node (LN) metastasis in human head and neck cancer (HNC) and identified algal methanol extract as a potential novel NRP2 inhibitor. METHODS: In silico analyses and immunohistochemistry were used to investigate the relationship between NRP2 expression and the prognosis of HNC patients. The functional role of NRP2 on the proliferation, migration, invasion, and cancer stem cell (CSC) properties of HNC cells was examined by MTS, soft agar, clonogenic, transwell migration and invasion assays, and sphere formation assays. Signaling explorer antibody array, western blot, and qPCR were performed toward the investigation of a molecular mechanism that is related to NRP2. RESULTS: NRP2 was highly expressed in HNC and positively correlated with LN metastasis and advanced tumor stage and size in patients. Using loss- or gain-of-function approaches, we found that NRP2 promoted the proliferative, migratory, and invasive capacities of human HNC cells. Furthermore, NRP2 regulated Sox2 expression to exhibit aggressiveness and CSC properties of human HNC cells. We demonstrated that p90 ribosomal S6 kinase 1 (RSK1) elevates the aggressiveness and CSC properties of human HNC cells, possibly by mediating NRP2 and Sox2. Zeb1 was necessary for executing the NRP2/RSK1/Sox2 signaling pathway during the induction of epithelial-to-mesenchymal transition (EMT) and aggressive behaviors of human HNC cells. Moreover, the methanol extract of Codium fragile (MECF) repressed NRP2 expression, inhibiting the RSK1/Sox2/Zeb1 axis, which contributed to the reduction of aggressive behaviors of human HNC cells. CONCLUSIONS: These findings suggest that NRP2 is a critical determinant in provoking EMT and aggressive behaviors in human HNC through the RSK1/Sox2/Zeb1 axis, and MECF may have the potential to be a novel NRP2 inhibitor for treating metastasis in HNC patients.

The Digastric Muscle: Its Anatomy and Functions Revisited / El Músculo Digástrico: Revisión de su Anatomía y Funciones

SUMMARY: As one of the suprahyoid muscles, the digastric muscle is characterized by two separate bellies of different embryologic origins. The origin of the anterior belly is the digastric fossa, while the origin of the posterior belly is the mastoid notch. They share a common insertion: the intermediate tendon. When the digastric muscle contracts, the hyoid bone is raised. Opening of the jaw and swallowing of food boli are associated with digastric muscle activity. This review discusses the general anatomic features of the digastric muscle and its variation, primary functions, and clinical implications focused on surgical reconstruction and rejuvenation.

Como uno de los músculos suprahioideos, el músculo digástrico se caracteriza por dos vientres separados, de diferentes orígenes embriológicos. El origen del vientre anterior es la fosa digástrica, mientras que el origen del vientre posterior es la incisura mastoidea. Comparten una inserción común, El tendón intermedio. Cuando el músculo digástrico se contrae, el hueso hioides se eleva. La apertura de la mandíbula y la deglución del bolo alimenticio se asocian con la actividad del músculo digástrico. Esta revisión analiza las características anatómicas generales del músculo digástrico y su variación, funciones primarias e implicaciones clínicas centradas en la reconstrucción y el rejuvenecimiento quirúrgico.

Surgical management and final outcomes of chondrosarcoma of the temporomandibular joint: case series and comprehensive literature review.

BACKGROUND: Surgical management for chondrosarcoma of the temporomandibular joint (TMJ) is challenging due to the anatomical location involving the facial nerve and the functional joint. The purpose of this case series was to analyze the largest number of TMJ chondrosarcoma cases reported from a single institution and to review the literature about chondrosarcoma involving the TMJ. METHODS: Ten TMJ chondrosarcoma patients at Seoul National University Dental Hospital were included in this study. Radiographic features, surgical approaches, histopathologic subtypes, and treatment modalities were evaluated. All case reports of TMJ chondrosarcoma published in English from 1954 to 2021 were collected under PRISMA guidelines and comprehensively reviewed. RESULTS: The lesions were surgically resected in all 10 patients with efforts to preserve facial nerve function. Wide excision including margins of normal tissue was performed to ensure adequate resection margins. All TMJs were reconstructed with a metal condyle except one, which was reconstructed with vascularized costal bone. At last follow-up, all patients were still alive, and there had been no recurrence. Among 47 cases (patients from the literature and our cases), recurrence was specified in 43 and occurred in four (9.5%). CONCLUSIONS: For surgical management of TMJ chondrosarcoma, wide excision must consider preservation of the facial nerve. Reconstruction using a metal condyle prosthesis and a vascularized free flap is reliable. A more conservative surgical approach correlates with a favorable prognosis for facial nerve recovery. Nevertheless, wide excision is imperative to prevent tumor recurrence. In cases in which the glenoid fossa is unaffected by the tumor, it is deemed unnecessary to reconstruct the glenoid fossa within an oncological setting.

Appropriate Total Rehabilitation in the Bilateral Maxillectomy Defected Diabetic Patient Secondary to Aggressive Aspergillosis.

Aggressive aspergillosis is a life-threatening fungal infection with rapid progress, mainly affecting the maxillofacial area, especially the nose and paranasal sinuses, in patients with immunocompromised conditions such as diabetes mellitus. Aggressive aspergillosis infection should be differentiated from other invasive fungal sinusitis for early recognition with correct prompt treatment. The main treatment is aggressive surgical debridement such as maxillectomy. Although aggressive debridement should be performed, preservation of the palatal flap should be considered for better postoperative outcomes. In this manuscript, we report the case of a diabetic patient with aggressive aspergillosis affecting the maxilla and paranasal sinuses and describe the appropriate surgical management and prosthodontic rehabilitation.

Adenoid Ameloblastoma Shares Clinical, Histologic, and Molecular Features With Dentinogenic Ghost Cell Tumor: The Histologic Spectrum of WNT Pathway-Altered Benign Odontogenic Tumors.

An epithelial odontogenic tumor called adenoid ameloblastoma (AA) has recently been included in the new WHO classification. However, AA has considerable overlapping features with a preexisting entity, dentinogenic ghost cell tumor (DGCT). This study compared the clinical, histologic, and molecular characteristics of AA and DGCT. Eight cases of odontogenic tumors initially diagnosed as AA or DGCT were included in this study. Quantitative histologic analysis, ß-catenin immunohistochemistry, and molecular profiling using next generation sequencing were performed. Additionally, accumulated clinical data of AA and DGCT were statistically analyzed. Nuclear ß-catenin accumulation was detected in all cases in common, although the tumors studied histologically consisted of varying combinations of the AA-like phenotype, ghost cells, and dentinoid. However, CTNNB1 hotspot mutations were not found in any case. Instead, loss-of-function mutations in tumor suppressor genes involved in the WNT pathway, including the APC, SMURF1, and NEDD4L genes, were found regardless of histologic type. In addition, KRT13 mutations were detected in 2 cases with a high proportion of ghost cells. Finally, a literature analysis revealed clinical similarities between the previously reported cases of AA and DGCT. These findings suggest that from a clinical and molecular point of view, AA and DGCT represent a histologic spectrum of WNT pathway-altered benign odontogenic tumors rather than 2 distinct tumors. Moreover, previously unidentified keratin mutations may be associated with ghost cell formation found in specific types of odontogenic lesions.

Clinical significance of L1CAM expression and its biological role in the progression of oral squamous cell carcinoma.

L1 cell adhesion molecule (L1CAM) has been implicated in the progression and metastasis of numerous cancers. However, the role of L1CAM in oral squamous cell carcinoma (OSCC) is not well characterized. In the present study, the expression of L1CAM was examined in oral tongue squamous cell carcinoma (OTSCC) tissue samples by immunohistochemistry, the clinicopathological significance of L1CAM expression was evaluated by chi­squared test, and the overall survival (OS) rate was analyzed using Kaplan­Meier method according to the expression of L1CAM. In addition, it was aimed to elucidate the biological role of L1CAM and the underlying molecular mechanisms by which L1CAM functions in OSCC cells in relation to epithelial­mesenchymal transition (EMT) and PI3K/AKT/ERK signaling pathways. Thus, the functions of L1CAM on the OSCC cell proliferation, migration and invasion, and the activation of EMT and PI3K/AKT/ERK signaling pathways were investigated in vitro. Positive L1CAM expression was found in 32.5% of OTSCC cases and was significantly correlated with high histologic grade, greater depth of invasion, lymph node metastasis, perineural invasion, advanced stage, and survival status. Patients with positive L1CAM expression had significantly lower OS rate. Particularly in patients with early OTSCC, L1CAM expression was strongly associated with worse prognosis. Overexpression of the recombinant human L1CAM protein significantly increased cell proliferation, migration and invasion. By contrast, L1CAM knockdown using small interfering RNA significantly inhibited cell proliferation, migration, invasion and EMT. Moreover, phosphorylated (p)­PI3K, p­AKT and p­ERK expression levels were significantly reduced by L1CAM knockdown. Taken together, the findings of the present study suggested that L1CAM could be a potential prognostic marker and a promising therapeutic target in OSCC.

Targeting tumor-intrinsic PD-L1 suppresses the progression and aggressiveness of head and neck cancer by inhibiting GSK3ß-dependent Snail degradation.

PURPOSE: PD-L1 is an immune checkpoint protein that allows cells to evade T-cell-mediated immune responses. Herein, we uncover a tumor-intrinsic mechanism of PD-L1 that is responsible for the progression and aggressiveness of HNC and reveal that the extracts of a brown alga can target the tumor-intrinsic signaling pathway of PD-L1. METHODS: The biological functions of PD-L1 in the proliferation and aggressiveness of HNC cells in vitro were examined by metabolic activity, clonogenic, tumorigenicity, wound healing, migration, and invasion assays. The clinical importance of PD-L1 in the prognosis of patients with HNC was analyzed by immunohistochemistry. The relationship between PD-L1 and EMT was confirmed via western blotting, qPCR, and immunocytochemistry. RESULTS: Through our in silico approach, we found that PD-L1 was upregulated in HNC and was correlated with an unfavorable clinical outcome in patients with HNC. PD-L1 was crucial for promoting tumor growth, both in vitro and in vivo. High expression of PD-L1 was closely correlated with LN metastasis in OSCC. PD-L1 facilitated the cytoskeletal reorganization and aggressiveness of HNC cells. Moreover, PD-L1 enhanced the EMT of HNC cells by regulating the Snail/vimentin axis. Consistently, MEIO suppressed the PD-L1/Snail/vimentin axis, thereby inhibiting the aggressiveness of HNC cells. Inhibition of PD-L1 induced by PD-L1 silencing or MEIO treatment caused Snail degradation through a GSK3ß-dependent mechanism. The tumor-intrinsic function of PD-L1 could be attributed to the regulation of the GSK3ß/Snail/vimentin axis. CONCLUSION: The discovery of MEIO targeting the tumor-intrinsic function of PD-L1 may prove particularly valuable for the development of novel and effective anticancer drug candidates for HNCs overexpressing PD-L1.

Prognosis of tongue squamous cell carcinoma associated with individual surgical margin and pathological features.

The specific muscular structure of the tongue greatly affects margin shrinkage and tumor invasion, making the optimal surgical margin controversial. This study investigated surgical margin correlated prognosis of TSCC (tongue squamous cell carcinoma) according to margin location and its value, and the histopathologic factors which are suggestive of tumor invasion. And we would like to propose defining of the surgical margin for TSCC via prognosis according to location and margin values. We reviewed 45 patients diagnosed with TSCC who visited Seoul National University Dental Hospital (SNUDH) (Seoul, Republic of Korea) from 2010 to 2019, who were managed by a single surgical team. Patient clinical and pathological data of patients were retrospectively reviewed, and in 36 out of 45 patients, the pathologic parameters including the worst pattern of invasion (WPOI) and tumor budding were investigated via diagnostic histopathology slide reading. When standardized with as 0.25 cm anterior margins, as 0.35 cm deep margin, there was no significant difference in disease specific survival (DSS) or loco-regional recurrence-free survival (LRFS). Additionally, there was a non-significant difference in DSS and LRFS at the nearest margin of 0.35 cm (PDSS=0.276, PLRFS=0.162). Aggressive WPOI and high tumor budding showed lower survival and recurrence-free survival, and there were significant differences in close margin and involved margin frequencies. In TSCC, the value and location of the surgical margin did not have a significant relationship with prognosis, but WPOI and tumor budding suggesting the pattern of muscle invasion affected survival and recurrence-free survival. WPOI and tumor budding should be considered when setting an optimal surgical margin.

Reappraisal of tubulopapillary hidradenoma-like tumor of the mandible: Suggested change in nomenclature to reflect tumor origin.

Several cases of intraosseous mandibular tumors have been reported under the name "tubulopapillary hidradenoma-like tumor of the mandible (TPHLTM)." However, the intraosseous occurrence of sweat gland tumors needs to be reappraised. The aim of this review was to propose a new name for these tumors to reflect the possible tumor origin. In view of the incidence and the tissue of origin, TPHLTM is more likely to be a salivary gland tumor than a sweat gland tumor. Among salivary gland tumors, a recently described salivary neoplasm called "sialadenoma papilliferum-like intraductal papillary tumor (SP-IPT)" seems to be histologically and genetically identical to tubulopapillary hidradenoma. Therefore, we proposed that the term TPHLTM be replaced by "SP-IPT of the mandible," which better explains its origin and could help in clarifying the nature of SP-IPT.

Surgical ciliated cyst of the mandible after orthognathic surgery: a case report with review of the literature.

BACKGROUND: Surgical ciliated cysts, also known as postoperative maxillary cysts or implantation cysts, occur mainly in the posterior maxilla after radical maxillary sinus surgery; they rarely develop in the mandible. They are thought to occur when the sinonasal epithelium is infiltrated by a surgical instrument during surgery or as a result of transplantation of bone or cartilage with respiratory epithelium attached. CASE PRESENTATION: We report a case in which a surgical ciliated cyst developed in the anterior part of the mandible, presumably as a result of bimaxillary orthognathic surgery and genioplasty performed 24 years earlier. We then review the few similar cases reported in the literature. CONCLUSION: Surgical ciliated cysts in the mandible are extremely rare, but they could occur after simultaneous surgery on the maxilla and mandible, even decades later. To prevent surgical ciliated cysts in the mandible, we recommend that the surgical instruments, especially the saw blade used during bimaxillary surgery, be new or cleaned and that previously placed plates and screws be removed at an appropriate time.

BRAF V600E and previously unidentified KRAS G12C mutations in odontogenic tumors may affect MAPK activation differently depending on tumor type.

Although several types of odontogenic tumors share the same mutations in MAPK pathway genes, their effects on MAPK activation remain unclarified. This study aimed to evaluate the associations between these mutations and ERK phosphorylation in ameloblastoma and mixed odontogenic tumors (MOTs) and to analyze the expression pattern of phosphorylated ERK (p-ERK) for determining the involvement of MAPK activation in the development and progression of odontogenic tumors. Forty-three odontogenic tumors consisting of 18 ameloblastomas and 25 MOTs were analyzed for BRAF, KRAS, and NRAS mutations by Sanger sequencing. The expressions of BRAFV600E protein and p-ERK were detected by immunohistochemistry. The associations between mutation status and p-ERK expression were statistically analyzed. The effect of BRAFV600E inhibition on MAPK activation was investigated in ameloblastoma cells. In benign MOTs, BRAFV600E mutations were neither expressed at the protein level nor associated with p-ERK expression. In contrast, BRAFV600E -mutant ameloblastic fibrosarcoma showed co-expression of BRAF V600E protein and p-ERK, especially in the sarcomatous component. In ameloblastoma, p-ERK was predominantly expressed in the tumor periphery showing a significant correlation with BRAFV600E mutations, and in vitro BRAFV600E inhibition decreased ERK phosphorylation. KRASG12C mutations, previously unidentified in odontogenic tumors, were detected in one case each of benign MOT and ameloblastoma; only the latter was high-p-ERK. In conclusion, unlike in benign MOTs, BRAFV600E and KRASG12C mutations lead to MAPK activation in ameloblastoma, suggesting their role as therapeutic targets. p-ERK intratumoral heterogeneity indicates that MAPK pathway activation may be associated with sarcomatous proliferation of ameloblastic fibrosarcoma and infiltrative behavior of ameloblastoma.

Effect of PAIP1 on the metastatic potential and prognostic significance in oral squamous cell carcinoma.

Poly Adenylate Binding Protein Interacting protein 1 (PAIP1) plays a critical role in translation initiation and is associated with the several cancer types. However, its function and clinical significance have not yet been described in oral squamous cell carcinoma (OSCC) and its associated features like lymph node metastasis (LNM). Here, we used the data available from Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), and Clinical Proteomic Tumor Analysis Consortium (CPTAC) to analyze PAIP1 expression in oral cancer. The publicly available data suggests that PAIP1 mRNA and protein levels were increased in OSCC. The high PAIP1 expression was more evident in samples with advanced stage, LNM, and worse pattern of invasion. Moreover, the in vitro experiments revealed that PAIP1 knockdown attenuated colony forming, the aggressiveness of OSCC cell lines, decreasing MMP9 activity and SRC phosphorylation. Importantly, we found a correlation between PAIP1 and pSRC through the analysis of the IHC scores and CPTAC data in patient samples. Our findings suggest that PAIP1 could be an independent prognostic factor in OSCC with LNM and a suitable therapeutic target to improve OSCC patient outcomes.

Primary intraosseous carcinoma in the pediatric and adolescent mandible.

BACKGROUND: Primary intraosseous carcinoma (PIOC) is a rare malignant odontogenic tumor that predominantly occurs in males older than 50 years. PIOC can be misdiagnosed as odontogenic cyst because it occasionally shows a well-defined border on radiography. In this study, related literatures of pediatric and adolescent PIOC cases were analyzed under strict PRISMA guidelines along with an adolescent case who was provisionally misdiagnosed as an odontogenic cyst. METHODS: All case reports for PIOC published in English from 1966 to 2021 were collected. Cases under the age of 20 were classified as pediatric and adolescent populations in this study. A total of 12 pediatric and adolescent cases including 11 PIOCs from the literature and one new case of a 14-year-old female were analyzed. Clinical and radiographic features, diagnosis and treatment approaches, and prognosis were investigated. RESULTS: Ages ranged from 4 to 18 years. The female to male ratio was 1.4:1. Seven cases occurred in the mandible. Swelling was observed in 11 patients. The radiologic borders were well-defined in six cases and corticated in four cases. Tooth displacement and root resorption were observed in four and six cases, respectively. The provisional diagnosis for seven patients was odontogenic cyst and enucleation was performed in six cases including the new case. During the follow-up period, local recurrence occurred in three patients. The pediatric and adolescent PIOC cases with local recurrence showed poor prognosis. The locally recurred lesion in the new case did not decrease in size despite concurrent chemo-radiation therapy. CONCLUSIONS: Three-dimensional imaging modalities and incisional biopsy with multiple specimens are necessary to rule out PIOC in the lesions with atypical radiographic findings. PIOC should be diagnosed differentially from odontogenic cyst even in pediatric and adolescent populations to properly manage the disease with poor prognosis.

Chronic Expanding Hematoma on Latissimus Dorsi Free Flap Donor Site Grown Over 17 Years.

ABSTRACT: The latissimus dorsi free flap (LDFF), that provides long vascular pedicle with rich vascularization and adequate bulk for maxillofacial defect coverage, is utilized in microvascular surgery for maxilla-mandibular reconstruction with high success rate, less morbidity, and ability to provide facial symmetry. In addition, it can reduce the risk of adjuvant therapies, such as radiotherapy. Seroma formation at the donor site following LDFF harvest has been reported as a common postoperative sequela. On the other hand, chronic expanding hematoma (CEH) in an LDFF donor site is a rare postoperative complication. in this case report, the authors describe a rare occurrence of a solidified CEH on an LDFF donor site in a male patient 17 years after mandible reconstruction surgery. For treatment, the patient underwent mass resection with drain placement and quilting suture, resulting in reduction of the hematoma and faster healing.

Odontogenic Keratocyst in the Masseter Muscle.

ABSTRACT: Odontogenic keratocyst (OKC) arising from purely soft tissue other than the mucosa covering the jawbone is rare. A 57- year-old Korean female patient presented with a lump on her right cheek, which had been suspected as a fibrotic mass on the buccinator muscle by the local clinic. Magnetic resonance imaging showed an ovoid mass in the buccal space just before the right ramus with an enhancing component in the marginal area, and the interior of the mass revealed a fluid signal. Histopathologically, the lesion showed the typical features of OKC and the cyst wall contained some daughter cysts and the minor salivary gland, muscle, and fat tissues. The authors report a very unique case of OKC arising in the masseter muscle.

Orthokeratinized odontogenic cyst: A large series and comprehensive literature review with emphasis on synchronous multiple occurrence and neoplastic transformation.

OBJECTIVES: The objective of this study was to demonstrate the clinical, radiologic, and histologic features of orthokeratinized odontogenic cyst (OOC); determine the characteristics of multiple OOCs; and present rare but significant manifestations of OOC. STUDY DESIGN: A clinical, radiologic, and histopathologic study of 65 primary and 2 recurrent OOC cases was performed retrospectively along with a comprehensive literature review. RESULTS: OOCs shared similar radiologic findings with odontogenic keratocyst, yet some showed features that have not been previously described: root resorption and radiopaque foci. Histologic review revealed a unique histiocytic lining and some findings suggestive of the multipotentiality of the odontogenic epithelium. The analysis of patients with multiple OOCs demonstrated that multiple OOCs occurred synchronously with a marked predilection for young male adults. Two unusual cases were also identified: an OOC combined with a BRAFV600E ameloblastoma and a recurrent OOC with malignant transformation. CONCLUSIONS: This largest series presents previously unreported radiographic and histopathologic features that can be seen in OOC. Multiple OOCs have clinical characteristics distinct from those of solitary cases. The first reported OOC associated with ameloblastoma suggests the involvement of oncogenic mutations in odontogenic tumorigenesis. Although OOC shows a low recurrence rate, the possibility of malignant transformation of recurrent OOCs should be emphasized.

Methanol extract of Sedum oryzifolium and its constituent, trehalose, impede the invasiveness of oral squamous cell carcinoma cell lines via downregulation of Slug.

BACKGROUND: Sedum species are reported to possess diverse pharmacological activities in various solid tumors. However, the anticancer functions of Sedum orizyfolium and its constituents have never been determined in human cancers. PURPOSE: The present study focused on addressing the inhibition efficacy of the methanol extract of S. orizyfolium (MESO) and its constituents and the molecular mechanism underlying invasion and epithelial-to-mesenchymal transition (EMT) in oral squamous cell carcinoma (OSCC) cell lines. STUDY DESIGN/METHODS: After MESO treatment, a wound-healing assay, an invasion assay, and immunocytochemistry were performed in OSCC cell lines, coupled with in silico analysis and immunohistochemistry in OSCC patient samples, to investigate the role of the EMT transcription factor Slug. Trehalose, an active component of MESO, was identified through gas chromatography-mass spectrometry. RESULTS: Among the methanol extracts of 18 various wild plants from South Korea, MESO exhibited the highest anticancer functionality in OSCC cells by downregulating Slug expression. In silico analysis and immunohistochemistry indicated that elevated Slug levels are remarkably associated with tumor progression and invasion in patients with OSCC, suggesting that changes in Slug expression alter EMT progression and invasion in OSCC. Notably, treatment with trehalose, a sugar component of MESO, inhibited invasiveness and Slug expression in OSCC cells. CONCLUSION: Cumulatively, this study highlighted the beneficial role of MESO and trehalose in the inhibition of invasiveness of OSCC cells via suppression of Slug expression and suggested a new design for potential chemotherapeutic drugs against OSCC.