Aging is a physiological change that leads to a decline in biological functions from metabolic stress. To investigate the effect of aging on mandibular bone formation, we created SAMP1/Klotho-deficient mice and performed micro-computed tomography (micro-CT) and histology analyses in 4-or 8 week-old SAMP1/kl -/- mice. SAMP1/kl -/- mice exhibited extensive inflammation, tissue calcification, and abnormal mandibular bone development. Using micro-CT analysis, SAMP1/kl -/- mice displayed a loss of incisor roots and irregular dentinal tubule formation, as well as calcification within the pulp root canal. Furthermore, the mandibular ramus showed extensive ground glass appearance in SAMP1/kl -/- mice. In histological analysis, we found calcified skeletal structures and dysplastic bone formation in SAMP1/kl -/- mice. These results provide an understanding of the pathologic alterations of aging-related mandibular bone. SAMP1/kl -/- mice may serve as a novel model for dysosteogenesis in mandibular bone development.

Ameloblastic fibrosarcoma (AFS) is an extremely rare malignant odontogenic tumor characterized with benign ameloblastic cells islands and malignant mesenchymal component. While two-thirds of AFS seem to arise de novo, but one-third develops from recurrent ameloblastic fibroma (AF) or ameloblastic fibro-odontomas (AFO). Pathological distinction of malignant transformation is essential for appropriate treatment. The patient was a 28 years old man. Since the primary tumor was excised, the mass recurred 2 years later. The recurrent tumor was diagnosed as AFS. Chief complaint was pain in the right mandible. Computer tomography finding revealed multilocular intrabony lesion with radiopaque substance in the primary lesion. In the recurrent lesion cortical bone destruction was found. Microscopically, both the primary and recurrent lesions showed benign ameloblastic follicles with myxoid or highly cellular mesenchymal proliferation. The histological difference between primary and recurrent lesions were that foci of dental hard tissue composed of enamel and dentin were found only in the primary lesion, whereas nuclear pleomorphism was aggrevated in the recurrent lesion. The histological criteria determining malignancy were discussed.

Nodular fasciitis is defined by the World Health Organization as a benign proliferative fibroblastic lesion. It was first described in 1955 by Konwaler et al. and also known as “nodular pseudosarcomatous fasciitis” and “infiltrative fasciitis”, which reflect the lesion’s rapid growth, dense cellularity, alarming mitotoic activity and lack of circumscription. Here, we report a case of nodular fasciitis, which appeared as subcutaneous mass of right perizygoma area in 40-year-old Korean female. She had no history of trauma or cosmetic surgery related with the lesion. She disclosed that the mass grew rapidly for last 2 months. Computed tomography showed relatively well-defined spherical mass with 1.2 cm in diameter. Under local anesthesia the mass was resected by intraoral approach. The histological examination revealed a relatively poor-dermacated mass with high cellularity, which was composed with infiltrative spindle-shaped cells without accompanying inflammatory reactions. The tumor cells were partially positive for α-smooth muscle actin and β-catenin, but negative for cytokeratin AE1/3, S-100, desmin, and CD34. Therefore, the lesion was pathologically diagnosed as nodular fasciitis. Although nodular fasciitis is known to pseudosarcomatous benign reactive lesion, the clinician need to follow up the patient periodically. The reasons are as follows; Nodular fasciitis may accompany nuclear accumulation of β-catenin, which imply neoplastic process rather than reactive process of the lesion. Moreover, it has many histological similarities with inflammatory myofibroblastic tumor which have malignant transformation tendency. Further research for mesenchymal tumor could help our understanding for the disease entity of nodular fasciitis

The osteoblastic activity of carcinoma is restricted in osteoblastic metastasis, common in the patients with prostate cancer, whereas its mechanism and the factors involved are unknown. Here, we present a case of central adenocarcinoma showing the osteoblastic activity in the mandible of the 80-year-old Korean male who had suffered from the paresthesia of lower lip during four mouths. Clinically the overlying oral epithelium was intact, but the radiologic images revealed the ill-defined radiolucent intraosseous lesions in left ascending ramus. Microscopically, the mandibular lesion was composed with carcinoma of ductal or glandular differentiation but lack typical features of any epithelial salivary gland malignancies. Intriguingly abundant new bone formation was found in the stroma, but the tumor cells expressed no reactivity for prostate-specific antigen(PSA). The patient had low ionized calcium level, normal serum alkaline phosphatase and PSA level. Positron emission tomography-computed tomopraphy scan revealed the benign prostatic hyperplasia, but failed to trace the primary site of tumor other than mandible. Therefore, pathologically diagnosis for the lesion was informed as adenocarcinoma, not otherwise specified(NOS). Because occult primary tumor associated with osteoblastic metastasis cannot be completely ruled out, periodic and careful check-ups for the patient should be performed.

Osteogenic sarcoma is primary malignant bone tumor. It can arise de novo or from the benign precursors lesions, like Paget’s disease, giant cell tumor, chronic osteomyelitis, osteoblastoma, and fibrous dysplasia. Here, we present a case of osteogenic sarcoma arising from florid osseous dysplasia appearing as a rapidly growing bony bulging mass in 44‐year‐old Korean female who had at first been non‐symptomatic, but later suffered from the numbness of chin and lower lip. The radiologic images revealed the mixed radiopaque‐ radiolucent intraosseous lesions throughout the mandible, which were diagnosed as florid osseous dysplasia pathologically. But only after 6 months, the lesions were substituted by the radiological ill‐defined diffuse bony sclerotic lesion with bone destruction, accompanying the interrupted periosteal bone formation, which were pathologically diagnosed as osteogenic sarcomas. These serial clinicopathologic changes imply the malignant progression of florid osseous dysplasia rather than the collision of benign condition, florid osseous dysplasia and malignant tumor, osteogenic sarcoma. The possibility for fibro‐osseous lesion of the jaw as premalignant lesion should not be overlooked; therefore, periodic check‐ups for the lesions are necessary. Proper evaluation and interpretation for clinical neural symptom and radiologic change of bone density may lead to the correct differential diagnosis and therapeutic intervention.

Epithelioid hemangioma is an unusual, which was at first described as angiolymphoid hyperplasia with eosinophilia (ALHE) in 1969 and misinterpreted as the same disease with Kimura’s disease. But now it represents a distinctive vascular tumor, a different entity with those inflammatory conditions. Here, we present a case of epithelioid hemangioma appearing as a diffuse gingival nodular mass in 33‐year‐old male who had suffered from the idiopathic sharp pain of left mandible area previously and later extended to left maxillary region, therefore the gingival lesion was clinically estimated as malignancy associated with neural invasion. CT images revealed the soft tissue mass restricted to left maxillary gingiva without infiltration to underlying maxillary alveolar bone. Histologically, the circumscribed soft tissue mass consist of solid sheets of epithelioid to spindled cells, expressing reactivity for neither cytokeratin AE1/3 nor HMB‐45, but for CD31, endothelial cell marker. Therefore, the lesion was pathologically diagnosed as epithelioid hemangioma. Diagnostic evaluation for the neurologic symptoms of the patient revealed the trigeminal neuralgia, accompanying with the present epithelioid hemangioma incidentally. Awareness of epithelioid hemangioma should be emphasized not to be misdiagnosed as malignant disease like an invasive squamous cell carcinoma, malignant melanoma, or angiosarcoma. Proper evaluation and interpretation for neural symptom may lead to the correct differential diagnosis and therapeutic intervention

Facial numbness restricted to the distribution of the mental nerve(mental neuropathy) is called "numb chin syndrome". The clinical importance of this syndrome is associated with first recognition of involvement of malignant diseases. The malignant neoplasm with numb chin syndrome show rapid progression and high mortality. We present a 43-year-old female who had been treated by radiotherapy for precursor T-cell leukemia/lymphoma involving the central nervous system( CNS) previously and later developed mental nerve invasion without central nervous system recurrence. MRI images revealed the CNS tumor mass remitted, and there was no identified peripheral nervous system(PNS) involvement including the mental nerve invasion, nevertheless the patient complained of consistent numbness and pain on right mandibular area. This is the first case of precursor T-cell leukemia/lymphoma accompanying mental nerve invasion without recurrence for central nervous system. Proper interpretation for mental neuropathy may lead to the prompt diagnosis and therapeutic intervention.

Epithelial-mesenchymal transition (EMT) can play an important role in carcinogenesis of oral squamous cell carcinoma (OSCC). EMT is characterized by morphological and phenotypical change of epithelial cells into mesenchymal cells, and transcriptional repressor of E-cadherin, Snail is critical for EMT. In order to investigate the role of Snail and E-cadherin in OSCC, we analyzed the immunohistochemical pattern of Snail and E-cadherin in 18 OSCCs. The expression of Snail in the OSCC was increased whereas the expression of E-cadherin in the OSCC was decreased in comparison with those of normal oral mucosa, showing reverse correlation. Especially, the fibroblasts near the islands of OSCC showed the positivity of Snail, suggesting the reactive fibroblasts to the EMT of epithelial tumor cells. In metastatic squamous cell carcinoma in cervical lymph node, the positivity of Snail of tumor cells was higher than that of primary OSCC. We concluded that the increased Snail expression and the decreased E-cadherin expression were involved in the progression, invasion and metastasis of OSCC.

Squamous cell carcinoma comprises about 95% of oral cancers. 까le gene디C 없mage in carcinogen-exposed fields is accumulated to transforrn norrnal mucosa in dysplas디c tissue and fmally invasive carcinoma through multistep process. This carcinogenic process has been a cause of the development of secondary tumors after the removal of primary carcmoma. πle improvement of therapeutic modalities of oral cancer has driven into the increase of multiple cancer occurrence in head and neck region. We experienced 3 pa디ents who had mul디ple squamous cell carcinomas in oral cavlty. π1ÎS study aimed to report multiple pr따laπ squamous cell carcinoma by clinical and pathologic examination and to discuss their molecular mechanism

Bisphosphonates have been widely used to treat metabolic bone diseases, although the . mechanism of bisphosphonate action on bone has not been fully understood. This study aimed to examine the direct action of pamidronate on cell proliferation and differentiation of cultured human mesenchymal stem cells(hMSC). Four experimental groups and two control groups were designed; Experimental groups included both osteogenic supplement(OS) and pamidronate-treated group, pamidronate-treated group after 1 week OS treatment, only pamidronate-treated group, OS-treated group after 1week pamidronate treatrnent. Control gr。니ps included DMEMtreated group and OS-treated group. Human MSCs were isolate from bone maπow ， and cultured for 7, 14, 21 days. For the detection of osteoblastic differentiation, AI.Pase activity was measured and the expression of type 1 collagen and osteocalcin were evaluated. Von Kossa’s silver stain was performed for the examination of calcification. As results, the proliferation rate of 바1SC was maintained to be more than 90% by 1uglml of pamidronate. AI.Pase activity showed the highest value at the concentration of 100nglml of pamidronate. In pamidronate-treated group, ALPase activity reached a peak at the third week and the expression of type 1 collagen mRNA and protein was enhanced compared to other experimental and control groups, whereas osteocalcin expression was found only in OStreated group. Calcification was decreased by a dose dependent manner followed by pamidronate treatment. This study su잃，est that pamidronate treatrnent may be able to enhance the osteoblastic differentiation of hMSC at the early stage. On the other hand, calcification appeared to be inhibited by pamidronate treatrnent.