The molecular mechanisms of the carcinogenesis of oral squamous cell carcinomas (OSCCs) are highly variable and result in different features of tumor progression, i.e., local tissue destruction and metastasis to regional lymph nodes. A case of OSCC arising from proliferative verrucous leukoplakia (PVL) was analyzed for its protein expression profile by immunoprecipitation (IP) – high performance liquid chromatography (IP-HPLC) by using 72 antisera and comparing results with those of KB cells. OSCC arising from PVL showed stronger expressions of proteins associated with cell proliferation (MPM2, PCNA, eiF5A, DHS, DOHH), cell survival (pAKT, MDM2, survivin), matrix proteolysis (elaffin), tumor suppression (p16, p21, PTCH1), the WNT/β-catenin pathway (SHH, WNT1, APC, β-catenin, snail), proinflammation (TNFα), angiogenesis (HIF, CMG2, vWF), and cellular protection (HSP-70, FAK, caveolin) and of oncoproteins (STAT3, 14-3-3, K-RAS, PUMA, PIM1) and growth factors (EGFR, bFGF) than KB cells. On the other hand, KB cells showed stronger expressions of proteins associated with apoptosis (caspase-3, caspase-8, caspase-9, PARP, FAS, FASL, TGase-1, BCL2, BAD, BID, BAK, FLIP), matrix proteolysis (MMP-2, MMP-9), transcription signaling (NFkB, p38, E2F-1, HO-1), and tumor suppression (p53, RB1, PTEN) and of oncoproteins (DMBT1, CEA) and growth factor (TGF-β1, c-erbB2, VEGF) than OSCC arising from PVL. These data indicate the cells of OSCC arising from PVL are more resistant and more robust than KB cells. Furthermore, they suggest the oncogenic signalings of OSCC arising from PVL play important roles in the aggressive growth and rapid tumor metastasis to regional lymph nodes

The prolonged bisphosphonate (BP) uptakes are frequently resulted in BP-related osteonecrosis of jaws (BRONJ). The previous study reported that the BP-involved bones were stained blue by Masson trichrome and showed weak birefringence compared to the normal bone1). Using the representative twenty cases of BRONJ osteomyelitis the present study examined the ultrastructure of BP-involved bone by scanning electron microscope (SEM) using decalcified bone microsections. As the BP-involved bones showed different features from adjacent normal bone by blue staining in Masson trichrome method and by rare birefringence under polarizing microscope, the ultrastructure of BP-involved bone matrixes were distinguishable histologically in comparison with normal bone. The normal bone showed the tight attachment of interdigitating dendritic bone matrixes, producing many Haversian canaliculi, while the BP-involved bone showed the compact alignment of granular bone matrixes, resulted in the abortive Haversian canaliculi. The osteocytes in the lacunar spaces of BP-involved bone became shrunken and necrotic, and the BP-involved bone showed many tunnel-like spaces produced by direct chemical resorptions and proteolytic degradation of bone matrixes. Taken together, it was conspicuous that the BP-involved bones were abnormal in their stainability of Masson trichrome, birefringence under polarizing microscope, and ultrastructure under SEM. These findings of BP-involved bone may have an implication for the pathogenetic roles of BRONJ, and can be applicable for the differential diagnosis of BRONJ from other osseous lesions.

The nasopalatine duct, the most dominant developmental tubule formed by the emergence of premaxilla and both sides of anterior palatal processes. This duct normally disappears in humans but remains latent and provides communication between the oral and nasal cavities in some mammals. However, the duct is obliterated and degenerated before birth in human, thus the persisting or patent nasopalatine duct in postnatal life is considered a developmental anomaly. Two cases of patent nasopalatine duct were presented in this study. Although the ducts were not sectioned longitudinally, they were probably connected each other and contained mucous materials secreted from the associated mucous glands. In the immunohistochemical study the ductal epithelium was consistently positive for the growth-related biomarkers including TGFβ1, c-erbB2, EGFR, CTGF, FGFb, HGF, eiF5A, FAK, and pAKT. And many columnar epithelial cells of the duct were positive for PCNA. Particularly, TNFα was clearly positive in the ductal epithelium together with β-defensin-2, -3 and MMP-3, -9. These findings may imply that the ducts have a growth potential postnatally and also can induce inflammatory reaction. Therefore, it was presumed that the present cases of patent nasopalatine ducts were caused by the latent proliferation of ductal epithelia in the vascular environment of nasopalatine canal without cyst formation, and also suggested that the patent nasopalatine ducts connected with functioning mucous glands were partly open to oral/nasal cavity and should be differentially diagnosed from the nasopalatine duct cyst.

A 72 years old male complained of gingival ulceration and whitish discoloration on the marginal and attached gingival epithelium of left mandibular premolar and molar area, where a porcelain-fused metal (PFM) crown and an ill-fitting gold crown were applied for 10 years, respectively. Recently he had a cancer phobia due to this whitish lesion unhealed even after intensive anti-inflammatory and antibiotic treatment. In the pathological examination the epithelium was hyperkeratotic and acanthomatous with severe inflammatory reaction, and subsequently its basement membrane was distorted and the intercellular spaces between keratinocytes were widened. Particularly, the nuclei of keratinocytes were elongated in the same direction towards the electric current between the dissimilar metallic crowns of PFM gold. In the immunohistochemistry KL1, β-catenin, and S-100 were strongly positive in the epithelium, but consistently weak for TNFα, HSP-70, and β-defensin-1, -2, -3. On the other hand, PCNA, p53, E-cadherin, and pAKT were rarely positive for the epithelium. Interestingly, the hyperkeratinized and inflamed epithelium was strongly positive for a calcium binding protein (S-100), while it showed almost reduced expression of protective molecules (HSP-70, β-defensin-1, -2, -3, and pAKT). Therefore, it was presumed that this localized lichenoid gingivitis was caused by the galvanic current phenomenon with lower cellular and immunological responses contrary to the ordinary oral lichen planus and leukoplakia

Oral erythroleukoplakia is characterized by severe dyskeratosis intermingled with multifocal erosive spots on the buccal mucosa, dorsal tongue, and lower lip, etc. A case of oral erythroleukoplakia was diagnosed among 83 cases of common oral leukoplakia since 1997. The pathological examination showed the typical features of leukoplakia with severe epithelial dysplasia, exhibiting dyskeratosis, acanthosis, and basal hyperplasia. The oral erythroleukoplakia was explored in comparison with a representative common oral leukoplakia by the immunohistochemical method using PCNA, β-catenin, EGFR, p53, TNFα, pAKT, and STAT3. Oral erythroleukoplakia showed strong positive reaction of PCNA, p53, EGFR, TNFα, pAKT1 and STAT3 in its spinous layer cells and these reactions were reduced in its basal layer cells, while common oral leukoplakia showed diffusely weak reaction of those proteins. Particularly, β-catenin was positive in the nuclei of some basal and spinous layer cells of oral erythroleukoplakia contrast to the common oral leukoplakia. These findings indicated that the present oral erythroleukoplakia was proliferative with the activation of β-catenin pathway, revealed the dysplastic changes of epithelium by the overexpression of EGFR, p53, and pAKT, and also produced inflammatory reaction through the activation of cytokine-dependent signalings of TNFα and STAT3. These data indicated that the present oral erythroleukoplakia might undergo the early stage of multi-step carcinogenesis via the overexpression of different oncoproteins, especially β-catenine, p53, pAKT, and STAT3.

Pemphigus is an autoimmune blistering disease characterized by autoantibodies against epidermal adhesion molecules, desmogleins. Pemphigus vulgaris is most common and shows intraepidermal vesicles caused by the breaking apart of epidermal cells, acantholysis. A 65 years old male patient complained of severe mucosa ulceration on his right mandibular retromolar pad area where traumatic injuries occurred during mastication. He also had multifocal round skin ulcerations, less than 7~8mm in diameter and showed habitual onset and disappeared soon. At this time he was anxious about his oral ulceration with a cancer phobia, thereby a biopsy was made to rule out any malignancy in the ulceration. The histology examination showed multifocal suprabasal splits forming vesicles and erosion. The suprabasal splits were linear and parallel to the basal cell layer. The immunostain of IgK was strongly positive in the vesicular fluid as well as the cell membranes of dissociating keratinocytes, and also positive in many plasma cells infiltrated into the subepithelial zone. TNFα, IL‐1, ‐8, ‐28 for the pro‐inflammatory reaction were weakly expressed, while IL‐6 was strongly positive in the acantholytic keratinocytes of vesicle forming area. β‐defensin‐1, ‐2, ‐3 for the innate immunity were diffusely positive in the involved epithelium. The cell survival proteins, pAKT and HSP‐70 were diffusely positive in the epithelium, while the apoptosis protein, PARP was consistently positive in some acantholytic keratinocytes. These findings indicated that the vesicle formation occurred by autoantibody reaction without the activation of pro‐inflammatory and cell‐mediated immune reactions. The lesion was diagnosed pemphigus vulgaris with abrupt onset of epithelial vesicles at the predisposing areas of traumatic injuries by type II hypersenstitive immune reaction.

Rushton bodies are known to be the aberrant keratinization and calcification in the epithelium of odontogenic cyst, which are similar to the features of calcifying odontogenic cyst and pilomatricoma. However, the pathogenetic mechanism of keratinization and calcification of Rushton bodies has not been clearly elucidated. Here, a case of Rushton bodies found in dentigerous cyst was examined by immunohistochemical method using antisera of PCNA, pAKT, HIF, PIM1, and PARP. The globular keratinization in lamellate fashion showed weak birefringency under polarizing microscope, and the Rushton bodies frequently underwent the dystrophic calcification. The polygonal keratinocytes of Rushton bodies were strongly positive for HIF and PARP, and the cyst epithelium was diffusely positive for pAKT and PIM1. Particularly, the cyst epithelium was hyperplastic and focally invaginated into cyst wall with positive reaction of PCNA. These findings may indicate the active response of odontogenic epithelium against the apoptotic stress of the cyst, producing the globular keratinization and irregular calcification in the polygonal keratinocytes. Therefore, it is presumed that the lamellate keratinization and dystrophic calcification of Rushton bodies are aberrant products of retrograding keratinocytes slowly undergoing apoptotic progresses similar to the phenomena of the ghost cells in calcifying odontogenic cyst and pilomatricoma, and also may have a potential for oncogenic proliferation.

Although the mechanism of the abnormal calcification in the calcifying odontogenic cyst (COC) was not elucidated so far, it has been known that the ghost cells are closely related to the calcification, producing dystrophic globular cementum-like materials, comparable to pilomatricoma in epithelium1). Here, we presented a case of COC occurred in left maxillary canine area of 23 years old female, exhibiting a collection of aberrant ossification admixed with basophilic ghost cells in comparison with seven cases of COC. In the polarizing microscope observation with Masson trichrome stain the present case clearly disclosed the typical birefringence of bony tissue, stained red in von Gieson stain, indicating the collagenous backbone. Some ghost cells showed the features of interdigitating epithelial attachments, empty spaces of nuclei, and reticular basophilic cytoplasms, which were similar to the basophilic ghost cells of philomatricoma. The present case demonstrated the aberrant ossification by basophilic ghost cells in COC similar to the ossification of pilomatricoma

Sparganosis is a rare parasitic disease caused by the infection of plerocercoid tapeworm larvae of the genus Spirometra. Up to date many cases of oral sparganosis had been diagnosed from biopsy specimens in Korea, however, in this study a 14 years old male showed an oral sparganosis in his buccal nodule producing its eggs, which were extruded through the ulcerated surface of buccal nodule. In the cytological observation for the pus‐like exudates many ovoid parasite eggs were found with a lot of inflammatory cells, which were mostly composed of eosinophilic polymorphonuclear leukocytes (PMNs). The eggs were measured about 50x50x80 μm, and had an operculum without opercular shoulder. In the subsequent biopsy examination the buccal nodule disclosed a diffuse granulomatous lesion with tunnel‐like spaces containing eosinophilic materials of parasite tegument, also infiltrated with a lot of eosinophilic PMNs. Therefore, we diagnosed it oral sparganosis producing its eggs with the characteristic features of sparganum granuloma in the cytological and histological observations, and also suggested that the cytological finding of parasitic eggs would be helpful to confirm the parasitic infection of sparganum matured enough to produce its eggs.

A 78 year-old male complained of mild pain at a gingival mass on his anterior mandible, injured and ulcerated by autobicycle accident six months ago. He had suffered from uncontrolled diabetes. The tumor specimens from his chin and gingiva were examined by immunohistochemical method, and their microsections showed poorly differentiated polygonal tumor cells, occasionally formed ductal structures. The tumor cells grew infiltratively into adjacent fibromuscular tissue with frequent atypical mitosis, exhibiting the features of poorly differentiated adenocarcinoma. However, in the computed tomography(CT) view a tumor mass was also found in his lung, and diagnosed lung cancer. In the immunohistochemical observation the tumor cells were strongly positive for thyroid transcription factor 1(TTF-1), cytokeratin 7, PCNA, p53, and PIM-1, occasionally positive for p63, but sparsely positive for survivin. The tumor cells were almost negative for S-100, cytokeratin 14, and α-SMA, while the vascular structures in the tumor tissue were conspicuously demarcated by the stains of α-SMA. Taken together, the present case was finally diagnosed poorly differentiated adenocarcinoma, metastasized from lung adenocarcinoma. And it was presumed that the metastatic tumor cells tended to be anchored in the traumatized area of anterior mandible, where the wound healing was undergoing with de novo angiogenesis and the activation of different cytokines and growth factors

A 17-year-old male patient was referred for the extraction of impacted mesiodens and canine (#23) before orthodontic treatment. In the radiologic examination, an ovoid-shape radiolucent lesion was found with well-defined hyperostotic rim involved the teeth in left maxillary area. After biopsy examination the lesion was diagnosed as glandular odontogenic cyst (GOC) differentially from non-odontogrnic cysts, i.e., nasopalatine duct cyst. In the immunohistochemistry the cyst epithelium was freguently positive for PCNA, clearly positive for amtloblastin, slightly positive for β-catenin, but rarely positive for amelogenin and cytokeratin 7. Mucin and PRP were positive in the secretory cells of the cyst epithelium. On the other hand, TNFα was strongly positive in the macropahges infiltrated into the mucin-filled cyst lumen, and CD68 and CD31 were positive in the mucin-filled macropahges. These findings may indicate that the glandular elements are derived from hamartomatous secretory organ and that this odontogenic cyst is arisen from the embryonal rests of enamel epithelium, which has a potential to be differentiated into not only the enamel organ but also the secretory gland. Taken together, we assumed that the present case of GOC was originated from the odontogenic epithelium of impacted teeth, but showed the cytodifferentiation of glandular cells.

Oral squamous cell papillomas(OSCPs) showed various features in their etiology, histology, and prognosis. Therefore, it is necessary to diagnose differentially according to their pathological examinations. In the present study total 14 cases of OSCPs were evaluated and characterized to be three types of OSCPs, i.e., papillary papilloma, verrucous papilloma, and inverted papilloma. The present study demonstrated that among 14 cases of OSCPs papillary papilloma (n＝6) showed the typical papillary projection of squamous epithelium with severe acanthosis of upper spinous layer cells, accompanying frequent nuclear vacuolization. And verrucous papilloma (n＝7) showed the diffuse acanthosis of whole spinous layer cells with severe basal hyperplasia, resulted in the thick squamous epithelium exhibiting verrucous surface and irregularly ingrowing rete pegs. One case of inverted papilloma showed the typical ingrowth of basal layer cells deeply into underlying connective tissue, resulted in the formation of multiple fissures on the surface area. The present study also revealed the predominant nuclear vacuolization suspicious for viral infection in papillary papilloma, and also heavy smoking history in the verrucous papilloma. On the other hand, as the epithelium of inverted papilloma ingrew into the underlying deep connective tissue up to the muscular layer, it is supposed that the inverted papilloma has a potential of basal layer proliferation strong enough to invade the protecting barrier of underlying connective tissue, or that the underlying connective tissue was too weak to prevent the ingrowth of basal layer epithelium. Taken together, because the OSCPs show heterogenous origins and variable pathological prognosis, it is suggested that the OSCPs should be differentially diagnosed at least into three types, i.e., papillary papilloma, verrucous papilloma, and inverted papilloma.

Socket sclerosis can be an obstacle for orthodontic space closure, however, the precise histomorphogenetic mechanism has not been elucidated up to date. A 73 years old female complained of dull pain on palpation in the extraction site of the left maxillary first molar, and uncomfortable to use her complete denture. In panoramic X-ray view the socket sclerosis was clearly demarcated as a radiopaque outline of extracted root. In histological examination the socket sclerosis showed the basophilic deposition of cementum- like materials in the peripheral rim of trabecular bones instead of eosinophilic osteoid materials for intramembranous ossification. In the immunohistochemical staining for osteogenetic proteins, BMP-2 was strongly positive in the peripheral rim of trabecular bone, in which RANKL and osteoprotegerin were also consistently positive. Particularly, versican, a marker of cementum was also positive in the peripheral rim of the trabecular bone. Therefore, it is presumed that the trabecular bones of socket sclerosis were hypermineralized by cementoid ossification, producing cementum-like materials by osteoblasts/cementoblasts derived from the previous periodontium.

Oral lichen planus (OLP) is an atypically keratinized and ulcerative lesion, producing severe pain and discomforts in the involved patients. Nevertheless, the etiological factor or the pathogenetic mechanism has not been clearly elucidated. In the present study, the different gene expressions were screened in 21 cases of OLP by immunohistochemical (IHC) array method using 80 antibodies, and found that the pathway of E-cadherin/β-catenin was abnormally expressed compared to the other essential genetic pathways. Particularly, the expressions of eIF5A, DHS, and DOHH, which are the biomarkers of protein translation, were remarkably reduced, nevertheless the expression of β-catenin was strongly positive in the 7 cases among 21 cases of OLP. The other expressions of p53, BCL-2, MDM-2, PAKT, BAX, BAK, BAD, NFkB, HO-1, etc, were usually weak or sparse, while the expressions of PCNA, CDK4, and HSP-70 were markedly increased. Taken together, it is presumed that the overexpression of β-catenin indicates the derangement of E-cad/β-catenin/NFkB pathway, causing the transcription of cellular proliferating genes in downstream events, i.e., PCNA and CDK4, and that it may be eventually relevant to the malignant potential of OLP epithelial cells. It is also suggested that the activation of β-catenin/TCF/LEF1 pathway be closely relevant to the immunological reaction of OLP with the accumulation of T-cells underneath the mucosal epithelium.

A 41-year-old male patient complained of a whitish growing mass on the central area of palate. The exophytic keratinizing mass was recently grown and showed rough surface localized at palatal mucosa. He has heavily smoked for more than 25 years. The lesion was clearly demarcated as an out-growing verrucous whitish epithelial lesion with erosive mucosa in the periphery and also continuous with the extensive hyperkeratosis in whole hard palatal mucosa. In the histological examination there appeared a plaque type verrucous hyperplasia in the absence of papillomatous growth. In the series of immunostains including PCNA, p53, β-catenin, APC, E-cadherin, BCL-2, MMP-1 and MMP-3 showed no features of infiltrative growth and malignant transformation. Therefore, the present case was diagnosed oral verrucous hyperplasia(OVH) different from squamous cell papilloma, verrucous leukoplakia, verrucous carcinoma, and oral squamous cell carcinoma.

Myositis ossificans traumatica(MOT) in head and neck area is a rare non-neoplastic, heterotopic bone formation within a muscle, arising after trauma or surgery. Although the several case reports have described the occurrence of MOT in other muscles of oro-facial musculature, MOT has never been reported in mentalis muscle. We demonstrate a case of MOT occurred in mentalis muscle of a 64 years old male. He recently complained of a movable mass with no pain. He had experienced a hitting trauma on his right anterior mandible about 25 years ago. Since then, the trauma area has been asymptomatic. The lesion showed severe muscular degeneration, resulted in a pseudocystic change without epithelial lining. The ectopic ossification was closely associated with the fibrous fascia of adjacent muscles. The lesion contained a lot of basophilic materials admixed with atrophying cells, which were supposed to be derived from muscle parenchyma injured previously. It was presumed that the basophilic materials induced callus-like ossification in the fibro-muscular lesion, also recruited macrophages and fibroblasts. However, the ossification processes in MOT were predominantly characterized by dystrophic calcification without osteoblastic differentiation of mesenchymal cells. Even more, there appeared some skeletal muscle bundles which were calcified dystrophically. Therefore, we suggest the present case of MOT might be initiated by dystrophic calcification in the degenerating muscle tissue

Glutamate-induced oxidative injury contributes to neuronal degeneration in many central nervous system (CNS) diseases, such as Parkinson’s disease, Alzheimer’s disease, epilepsy and ischemia. Inducible heme oxygenase (HO)-1 acts against oxidants that are thought to play a role in the pathogenesis of these diseases. The EtOH extracts of Viola mandshurica (NNMBS274), Viola patrinii (NNMBS275) and Viola papilionacea Pursh (NNMBS276), origin plants of Violae Herba, showed the potent neuroprotective effects on glutamate-induced neurotoxicity. Among them, NNMBS275, the extract of V. patrinii possessed the protective effects against glutamate toxicity by inducing the expression of heme oxygenase (HO)-1 in the mouse hippocampal HT22 cells. These results suggest that extracts of V. patrinii could be the effective candidates for the treatment of ROS-related neurological diseases. Furthermore, it is suggested that the protective effects of V. patrinii extract due to inducing the expression of HO-1 asAs the exfoliated keratinocytes (EKs) in oral mucosa are aging and degenerating cells, of which cytoplasms are almost replaced by cross-linked keratin materials. Consequently, the EKs become apoptotic with nuclear lysis. A question is arisen what is the biological role of these EKs in oral cavity? Are they simply degrading as aging keratinocytes or do they have some essential function still remained in the exfoliated status? The buccal smear samples from ten healthy adult subjects were observed under scanning electron microscope. On the outer surface of the EKs the features of bacterial adhesion were explored. The microorganisms attached on the surface of EKs were much deformed, shrunken and teared. Only a few microorganisms were found on the EK surface, aggregated focally. The attached microorganisms were gradually fused on the cell membrane of EKs, and subsequently endocytosed. Resultantly, many round endocytotic concave cavities similar size to the cocci were remained on the surface of EKs similar to the sequels of caveolae endocytosis. These data indicate that the degenerating EKs can actively engulf microorganisms attached on their cell surface via the processes of caveolae endocytosis. Therefore, it is presumed that the oral EKs still play a role for endocytotic scavenging of oral microorganisms using the denatured cell bodies themselves, which become highly adherent to oral microorganisms and still function for caveolae endocytosis in mixed saliva environment. an antioxidant/cytoprotective target

Human pituitary tumor transforming gene 1 (PTTG1), which is a newly identified proto-oncogene, is highly expressed in normal pituitary tissues containing proliferating cells and in several cancers. Also, PTTG1 has been known as a securin to involve in the regulation of c ell-cycle and in t he p rogression o f tumor. B u t the effect o f PTTG1 in o ral squamous cell carcinoma (oral SCC) h as not b een studied yet. The objective of this study is to analyze the expression of PTTG1 in oral SCC cell lines (YD-10B and YD-15) and to evaluate the effect of PTTG1 on oral SCC cell lines for the migration effect by PTTG1 siRNA treatment. Western blot, migration assay, and zymography were performed to evaluate the effects of PTTG1 on the expression of MMP-2/-9 and migration activity after PTTG1 siRNA treatment. PTTG1 was expressed in oral SCC cells lines, otherwise, significantly decreased after PTTG1 siRNA treatment. There is no difference in expression of MMP-2 regardless of PTTG1 siRNA treatment. However, the enzyme activity of MMP-9 was significantly decreased. In addition, the migration activities of oral SCC cells were significantly decreased after PTTG1 siRNA treatment (p<0.001). These results suggested that the down-regulated PTTG1 could inhibit the migration of human oral SCC cells through the low MMP-9 expressions. Therefore, these findings provide a useful guideline for the migration mechanism of oral SCC depend on PTTG1 expression.

The present case occurred in the cervical area of 51 years old male, who was generally healthy but recently complained of cervical swelling with mild pain. The tumor recently grew rapidly for 5 months. He was referred from local hospital in the diagnosis of metastatic tumor in cervical lymph. In the biopsy procedure, the tumor mass was ill-defined and not associated with cervical lymph node. The microsection showed a highly proliferative fibrous tissue infiltrative growth into the periphery. The spindle tumor cells were stained red in Masson trichrome stain, and strongly positive for PCNA and β-catenine, and partly positive for α-smooth muscle actin (α-SMA), but negative for S-100 and desmin. The differential diagnosis in primary biopsy examination was made as leiomyosarcoma, malignant schwannoma, and mesenchymal sarcoma. Under the diagnosis of sarcoma the patient was operated for tumor resection including cervical lymph nodes. The tumor mass was tightly attached on the lower border of left mandibular body. After the surgical operation the tumor tissue was more investigated with further immunohistochemical stainings, and discussed with several pathologists in Gangneung area. Finally the tumor was turned out to be a nodular fasciitis with pseudosarcomatous proliferation, and also confirmed that the pseudosarcomatous spindle cells belonged to the myofibroblasts originated from the fibrovascular fascial tissue. The present study demonstrated a rare case of nodular fasciitis, which should be differentially diagnosed from the malignant head and neck tumors.

To evaluate the biohazard properties of an extremely low frequency electromagnetic field (ELF-EMF), we explored the physical properties of the ELF-EMF that generates the electric current induction in the secondary coil from the chamber of a primary solenoid coil. We subsequently explored the biological effects of a strong alternating electromagnetic field (EMF), ranging from 730-960 Gauss, on the mouse testis. Mice were exposed to an alternating EMF field induced by a rectangular electric current at 1, 7, 20, 40, and 80 Hertz, for 1, 3, 5, and 7 hours. The mouse testes were examined for proliferative activity and apoptosis using the in situ terminal deoxynucleotidyl transferase (TdT) method and by immunostaining of proliferating cell nuclear antigen (PCNA), respectively. We found that the electric currentm induction increased in the 6-8 Hertz range, and that exposure to an ELF-EMF induced the apoptosis of mouse spermatocytes. In situ TdT staining was found to be most prominent in 7 Hertz group, and gradually reduced in the 20, 40, and 80 Hertz groups. These data suggest that a strong EMF can induce reproductive cell death within a short time, and the harmful effects of the EMF are maximal at low frequency alternating EMFs.