Osteoblastoma is a benign bone forming neoplasm most commonly occurring in the vertebrae, long bones, but the jaw involvement is very rare events. When localized close to the periapical region or laterally to the roots of the t eeth, the lesion is easily confused with inflammatory periapical pathosis. In this article, we report our experience with a case of osteoblastoma located in the periapical region that was initially misdiagnosed as an inflammatory periapical pathosis, which led to unnecessary dental treatment and a delayed diagnosis. This case demonstrates the importance of proper diagnosis and treatment planning when one is dealing with radiolucent lesions in the periapical area Therefore, this case stresses the importance of biopsy of periapical lesions that do not respond to endodontic treatment or are otherwise S USpl CIOUS.

T:raumat ic eosinophili c granuloma(TEG) of the oral mucosa is considered to be a reactive benign lesion. which commonly manifests as an ulcer with elevated and indurated borders Clinically, this lesion simulates a malignant tumor. Histology shows a diffuse. dense, polyrnorphic, and eosinophil - rich cellular infiltra te. which extends deeply into the underlying soft t issues. A major constituent of infil trates is a population of mitotically active‘ la rge‘ atypi cal mononuclear cells. Immunohistologic evaluation of the large atypical cells has suggested a myofibroblastic 01' his tiocytic ol'igin. However, recent reports have shown that these cells are positive 1'01' CD30 antigen and it has been s llggested tha t a subset of TEG cOllld be included within the spectrum of CD30+ lymphoprolifer ative disorders. We have described 2 patients who had oral mllcosal lesions with features of TEG. ln patient 1. the lesiona l cells expressed CD3 .. CD43, LCA. Interestingly, the large cells were strongly CD30 positive. bl1t nega tive for CD68, CD45Ro‘ CD56, CD20. This case was interpreted as a CD30+ Iymphoproliferative disorder. In pa tient 2‘ t he la rge cell s showed strong posit ive for CD68, hut negative for CD30 The small lymphocytic cells ex prerssed CD3 This case was interpreted as an atypical histiocytic granuloma. Therefore, TEGs inclllde atypical histiocytic granllloma a long with the CD30+ lymphoid lesions. These findings suggested that TEG w0111d be a hete rogenous category of oral mucosal di sorders

It has been reported that light-emitting diodes(LED) can be used in the treatment of oral diseases. Although bio-stimulatory effects of LED irradiation such as promotes stimulation of wound healing have been well known, there are few reports about molecular mechanism associated with cell cycle by LED irradiation. The purpose of present study was to examine the molecular event in cell cycle of LED irradiation on primary human gingival fibroblast(hGF) in vitro. The source of light for irradiation was a continuous-wave LED emitting at a wavelength of 635nm, and manufactured that energy density was 5mW/cm2 on sample surface. The hGF were irradiated for 1 hour at 37℃ in 5% CO2 humidified chamber. Experimental samples were acquired at 0 (right after irradiation), 8 and 24 hour after irradiation. To investigate the molecular mechanisms associated with cell cycle, growth phase was determined by flow cytometry and mRNA expression of cyclin A, cyclin B, cyclin D1, cyclin E, cdc2, PCNA, p18, p27, p21, and p53 were determined by real time RT-PCR. Flow cytometric analysis demonstrated the percentage of cells in the G1 and S phase were decreased, but the G2 phase increased, which showed cells irradiated by LED were transitioned from S to G2 phase. For mRNA expression, cyclin B, cdc2, PCNA and p53 were increased at 0 hour after irradiation, and most of cell cycle molecules were increased at 8 hour after irradiation. At 24 hour after irradiation, cyclin A, cyclin E, PCNA and p18 were increased. Taken together, LED irradiation induced proliferation of hGF cells through transition from S to G2 phase.

Hereditary dentin defects consists of dentin dysplasia(DD) and denti nogenesis imperfecta(Dr) ‘ The Dl associated with osteogenesis imperfecta has been classified as DI type 1. whereas isolated inherited defects have been categori zed as DI types II and III , However‘ whether DI type III should be considered a distinct phenotype 01' a variation of DI type 1I is debatable , Recent genetic findings have focused attention on the role of the dentin sialo phosphoprotein(DSPP) gene in the etiology of inherited defects of tooth dentin, We have identified novel mlltation( c,727G - > A, p,D243N) at the 243th codon of exon 4 of the DSPP gene in a Korean patient with DI type III The radiographic and histologic features of the patient revealed the classic phenotype of shell teeth These findings sllggest that DI type II and III are not separate diseases bllt rather the phenotypic variation 01' a s ingle disease