Anchorage plays an important role in orthodontic treatment. Recently, some clinicians have tried to use skeletal anchorage system(titanium miniscrews and microscrews) in treatment due to their many advantages such as ease of insertion and removal, low cost, immediate loading, and the ability to place miniscrews in any area of alveolar bone. The purpose of this study was to investigate the histopathologic change of alveolar bone density around miniscrew under variable ortho -donticforceinyoung-adultdogs, throughthepolarizingmicroscopic findings. For this study, three young adult mongrel dogs(6-months in age) were used, 12 titanium miniscrews were inserted into the palatal bone(4 miniscrews placed in each dog), and then miniscrews were loadedwithorthodonticforce [50gm(F1),100gm(F2),250gm(F3), 500gm(F4)] immediately after implantation. After 1, 3 and 6 weeks, the animals were sacrificed. Then the miniscrews and surrounding bone of dogs were removed, respectively. The grinding samples along the long axis of miniscrew were made. The changes of bone density and thrombosis were examined under the polarizing microscope. Bone density was determined as color changes. The results of this study were as follows.
1. There was no thrombosis in the F1 group. But thrombosis was seen in 1 week of T side, 1, 3, 6 weeks of P side in
the F2 group, 1, 3 weeks of T side, 1, 3, 6 weeks of P side in the F3 group and 1, 3, 6 weeks of both P and T side
in the F4 group.
2. The changes of bone density decreased in P side more than T side in 1 week, while more decreased P side in 3
weeks than 1 week. In 6 weeks, bone density more increased in T side than P side along the middle & apex.
3. As orthodontic force increased, there was severe thrombosis, especially in cervical of P side. As it went up to 3, 6
weeks, thrombosis was decreased but remained.
4. As orthodontic force increased, bone density more severely decreased due to bone destruction in 1 and 3 weeks,
but more slowly increased due to bone formation in 6 weeks.
Based on the results of this study, in the practice, because of optimal orthodontic force for the most of tooth movement was less than 150gm, I thought that miniscrews could play role of use of skeletal anchorage immediately after implantation. In the more than 250gm & 500gm of orthodontic force, I thought that miniscrews would be delayed as use of skeletal anchorage after loss of bone was restored.
The purpose of this study was to evaluate the role of EGF(Epidermal Growth Factor), EGFR(Epidermal Growth Factor Receptor), aFGF(acidic Fibroblast Growth Factor, FGF-1), bFGF(basic Fibroblast Growth Factor, FGF-2), FGFR(Fibroblast Growth Factor Receptor) in the development of radicular cyst. For this study 37 subjects, diagnosed as radicular cysts. referred to the Dept. of Oral Path. College of Dentistry, Kyung Hee University, were used as experimental group. And for control group, 2 subjects of normal oral epithelium without any inflammatory changes were used. All the tissues; experimental and control group were neutral formation fixed and paraffin embedded. serial tissue section were made at 5㎛ and processed in the standard way for immunohistochemical method, using primary antibodies against, EGF(Antirabbit Ig G at 1:100 dilution), EGFR(Antimouse Ig G at 1:100 dilution), aFGF(Antirabbit Ig G, rabbit kit at 1:100 dilution), bFGF(Antirabbit Ig G, mouse kit at 1:100 dilution), FGFR(Antimouse Ig G mouse kit at 1:100 dilution), all BioGenex U.S.A. made except EGFR(Chemicon U.S.A.) followed by the Streptavidin - Horse Radish Peroxidase (InnoGenex Human-avidin kit) application, counter stained with Meyer's hematoxylin stain method. And examined under microscope, graded 0(no epithelial stain), +(weak or focal epithelial stain), ++(moderate or focal intensive epithelial stain), +++(intense generalized epithelial staining) for the epithelium, and connective tissue of cyst wall.
1. EGF, EGFR, aFGF, bFGF, FGFR showed more intense staining on radicular cysts compare to that on the normal
2. EGF, EGFR, aFGF, bFGF, FGFR stained in mucosa, submucosa of the control group and also stained on the lining
epithelium, connective tissues of cyst wall in the experimental group.
EGF, EGFR, aFGF, bFGF, FGFR take a part in the development of the radicular cyst.
p16INK4A and p15INK4B tumor suppressor genes are frequently altered in various human tumors. Hypermethylation of the promoter region of p16INK4A and p15INK4B seem to be the major mechanism of inactivation. To determine whether the change in p16INK4A and p15INK4B methylation status occur in oral squamous cell carcinomas (OSCCs) and benign oral epithelial hyperplasias, we analyzed 46 OSCCs and 20 benign oral epithelial hyperplasias by methylation-specific PCR. We also analyzed a subset of the samples for p16INK4A and p15INK4B protein expression by immunohistochemistry. The promoter region of p15INK4B was hypermethylated in 13 specimens of the 15 finally analyzed OSCCs and three specimens of the five analyzed benign oral epithelial hyperplasias. By immunohistochemical analysis, we confirmed the loss of p15INK4B expression of all hypermethylated specimens. The promoter region of p16INK4A was amplified by both an unmethylated- and a methylated-specific primers in just one OSCCs. The remaining specimens including 11 OSCCs and four benign oral epithelial hyperplasias were normally methylated. By immunohistochemistry, we analyzed the loss of p16INK4A expression in seven specimens of the 12 OSCCs and two specimens of the four benign oral epithelial hyperplasias. Except for one OSCC, however, all specimens showing loss of expression were normally methylated. These results suggest that loss of p16INK4A and p15INK4B protein expression play an important role in the development of both OSCCs and benign oral epithelial hyperplasias.
be involved in the development of oral SCC. If we compare the morphologic features of NHOK to IHOK according to calcium concentration by TEM, IHOK have been gained wide acceptance as a model system for HPV-linked oral carcinogenesis. We already have established immortalized oral keratinocytes(IHOK) transfected by E6 and E7 gene. The purpose of this study were to examined the ultrastructural features of cultured NHOK, IHOK, and HN4 oral squamous cell carcinoma cell line, and to apply these results to oral carcinogenesis in the future. NHOK from healthy retromolar pad was primarily cultured at 37oC and 5% CO2. IHOK, and HN 4 cell line which were cultured under 0.15 and 1.2mM Ca++ of KBM bullet kit. For transmission electronmicroscopy(TEM), under preconfluency, and after 3 days of postconfluency under 1.2mM Ca++, cultured NHOK, IHOK, and HN4 cell line were immediately fixed in 2.0% glutaraldehyde in 0.1M cacodylate buffer(pH 7.4) at 4OC for 1h. The ultrathin sections were stained with uranyl acetate and lead citrate, and examined by TEM. The obtained results were as follows.
1. TEM of cultured NHOK under 1.2mM Ca++ showed increased tonofilaments, and vaculated ovoid cells with cornified envelope, while cultured IHOK showed prominent microvilli, unilateral desmosome in microvillus, and tonofilaments.
2. TEM of HN 4 cell line sowed numerous microvilli, increased N/C ratio, and lateral desmosome in microvilli under 0.15mm, while under 1.2mM well forming desmosomes.
From the aboving results, under high calcium cultured IHOK showed less tonofilaments than that of cultured NHOK, while cultured IHOK, and HN 4 cell lines showed more increased desmosomes under high calcium. It was suggested that the ultrastructural changes of cultured IHOK would be accepted as intermediate stage cells for studying oral carcinogenesis.
We used three-dimensional Matrigel culture system to examine the morphognesis of normal and malignant salivary glands cell in vitro including acinar cells(AC), myoepithelial cell(MC), salivary gland adenocarcinoma cells(SGT), mucoepidermoid carcinoma cells(MEC), and immortalized human salivary gland cells(HSG). For this purpose, normal and salivary gland tumor cells cultured in 3-D Matrigel, and characterized histologically and immunohistochemically, compared with same cells grown on monolayer culture and patient tissue from biopsy.
1. In three-dimensional Matrigel culture, HSG cells form acinar structure, SGT cells shows duct like structure, and other AC, MC and MEC cells dont' form any structure , and their morphology was different from that of monolayer cells.
2. Matrigel involved cell proliferation at a similar pattern to cells on plastic monolayer cell cultures, and monolayer cell revealed higher cell viability than that of Matrigel cultured cells.
3. All salivary glands cells on Matrigel or monolayer showed strong PCNA expression, and there is no expression difference in these cells. But some cells including myoepithelial cells in normal and salivary gland tumor tissue showing PCNA lavelling, so there is PCNA expression difference among normal and tumor tissue cells.
4. Actin expression was noted in AC cells on Matrigel, were rare expressed in the other cells except in MEC cells, and was present in myoepithelial cell and ductal cells of normal gland tissue. There is actin expression difference between tissue and cultured cells .
5. S-100 immunoreaction was moderateively positive in MC cells of monolayer culture, myoepithelial cells of normal tissue and pleomorphic adenoma, all cancer cells of mucoepidermoid carcinoma tissue, but significantly decreased in all salivary cells on Matrigel.
6. TGase 2 expression was prominent in MC cells of monolayer and Matrigel cultured, in myoepithelial cells of normal gland and pleomorphic adenoma, epidermoid cells of mucoepidermopid carcioma, and strong reaction in MEC and AC cells of monolayer and Matrigel cultured.
7. Expression of CK in monolayer culture showed strong reaction to CK6 in all sailvary gland cells, and mild reaction to CK10 and CK16 for all salivary cells, CK16 and CK19 expression in monolayer culture was similar to that of Matrigel culture.
8. CK6 and CK10 expression was strongest in AC and MC cells on Matrigel, and CK 4 was negative reaction in AC, SGT, MEC cells, strong reaction in MC cells but mild in SGT cells on Matrigel. Expression of CK was rare in HSG cells compared with other salivary gland cells, CK16 was prominent in SGT cells, CK10 and CK16 showed strongest expression in MEC cells of Matrigel.
9. Monolayer culture of HSG cell shwoing strong reaction to CK6, moderate to CK19 and mild to the others CK, but 3D cultured HSG cells reveal mild expression to CK16, and rare to others CK, intercallated duct in normal gland tissue showing strong to CK19, and mild to the others Ck, so there are CK expression difference in tissue, monolayer and 3-D cultured cells.
10. Monolayer culture of MEC cells represent strong reaction to CK6, mild to other CK, 3-D cells showing increased CK expression including CK6, epidermoid cells and intermediate cells in mucoepidermoid carcinoma tissue reveal positive to CK6 and CK16, mucous cell positive to CK10 and CK19, so Matrigel showed similar CK pattern
compared to mucoepidermoid carcinoma tissue rather than monolThese data indicate that the interaction of salivary gland cells with basement membrane is an important factor in salivary gland development and cytodifferentiation, so this model system will be useful to study acinar or ductal differentiation in vitro.ayer cultred.
For the safety extirpation in case of acute pulpitis with painless procedure, lots of pulp devitalizers have been designed for a long time. Authors have manufactured experimental pulp devitalizer with adding some other constituents for main components of paraformaldehyde and local anesthetics. The purpose of this study was to observe the histopathologic tissue response in pulp tissues by applying newly developed safety pulp devitalizer to the human tooth. For this experiments 5 human teeth in 4 patients (ages of 26 to 49) were used. In case of acute pulpitis with pulp exposure, divided into two groups; One group, carious dentin removed, and then was applied newly developed devitalizer directly to exposed small pulp tissues. Other group, was exposed the pulp chamber, pulpotomized and then the devitalizer was applied to remaining pulp tissues. The teeth were extracted on 3rd and 7th day after operation respectively. For the control group, Depulpin? was used as pulp devitalizer. All the extracted teeth were fixed in 10% neutral formalin solution, decalcified in Plank-Richlo solution, embedded in paraffin, sectioned 6-8㎛ in thickness, stained with hematoxylin-eosin stain method, and examined under microscope. Attained results were as follows;
1. There were no difference in histopathologic aspects either exposed or not pulp chamber, the extent of necrosis of pulp tissue and destruction of odontoblast was similar to that on the 3rd day of control group and both the 3rd and 7th day of the experimental group.
2. For the necrosis of pulp tissue and destruction of odontoblast on the 3rd day of control group exposed pulp chamber, was similar to that on the 3rd day of experimental group exposed small pulp tissue. The experimental pulp devitalizer could reduce the side effects, which reduced the amount of paraformaldehyde components, adding other constituents, reduced the duration of pulp devitalization, and useful whether exposed or not the pulp chamber.