Toshio Sugahara

Factors associated with the stability of titanium screws placed in the posterior region for orthodontic anchorage

Recently, implant anchors such as titanium screws have been used for absolute anchorage during edgewise treatment. However, there have been few human studies reporting on the stability of implant anchors placed in the posterior region. The purpose of this study was to examine the success rates and to find the factors associated with the stability of titanium screws placed into the buccal alveolar bone of the posterior region. Fifty-one patients with malocclusions, 134 titanium screws of 3 types, and 17 miniplates were retrospectively examined in relation to clinical characteristics. The 1-year success rate of screws with 1.0-mm diameter was significantly less than that of other screws with 1.5-mm or 2.3-mm diameter or than that of miniplates. Flap surgery was associated with the patients discomfort. A high mandibular plane angle and inflammation of peri-implant tissue after implantation were risk factors for mobility of screws. However, we could not detect a significant association between the success rate and the following variables: screw length, kind of placement surgery, immediate loading, location of implantation, age, gender, crowding of teeth, anteroposterior jaw base relationship, controlled periodontitis, and temporomandibular disorder symptoms. We concluded that the diameter of a screw of 1.0 mm or less, inflammation of the peri-implant tissue, and a high mandibular plane angle (ie, thin cortical bone), were associated with the mobility (ie, failure) of the titanium screw placed into the buccal alveolar bone of the posterior region for orthodontic anchorage.

Suppressive effect of overexpressed connective tissue growth factor on tumor cell growth in a human oral squamous cell carcinoma-derived cell line

Connective tissue growth factor (CTGF) is known to be a multifunctional growth factor that is overexpressed in several types of malignancies. In this study, effects of CTGF gene overexpression on the phenotypes of oral squamous cell carcinoma cells were investigated by using a cell line with undetectable endogenous CTGF expression. Surprisingly, our results indicated that CTGF-overexpressed clones were characterized by attenuated cell growth and less potent tumorigenicity, with coincidental downregulation of prothymosin alpha gene. Although CTGF is known to promote cell proliferation in mesenchymal cells, our present results suggest that CTGF acts as a negative regulator of the cell growth in oral squamous cell carcinoma possibly through its interaction with growth modifiers inside the cell.

Interaction of AP-1 and the ctgf gene: a possible driver of chondrocyte hypertrophy in growth cartilage

Abstractu2003The expression of the connective tissue growth factor (ctgf) gene increases along with the differentiation of growth cartilage cells, and the highest expression is observed in the hypertrophic stage. Similarly, recent reports demonstrated c-fos expression in chondrocytes in the early hypertrophic zone of growth cartilage, and suggested that the c-fos gene may play a crucial role in the regulation of hypertrophic differentiation. A chondrocytic human cell line, HCS-2/8, is known to retain a variety of chondrocytic phenotypes. When such cells were kept overconfluent, they expressed increasing levels of c-fos transcripts along a time course phenotypically similar to that of hypertrophic differentiation. Moreover, by using a competitive electromobility-shift assay, we found that AP-1, a Fos/Jun heterodimer, in HCS-2/8 was capable of binding not only to a typical AP-1-binding DNA fragment but also to the enhancer fragment of the ctgf gene. Based on the findings above, we hypothesize that, prior to hypertrophic differentiation, AP-1-related oncogenes are activated and that their gene products subsequently activate ctgf gene expression, which might eventually induce hypertrophy.

Pathology of the temporomandibular joint of patients with rheumatoid arthritis–case reports of secondary amyloidosis and macrophage populations

INTRODUCTIONnThe pathogenetic features of rheumatoid arthritis of the temporomandibular joint (TMJ) are not well defined. In this paper the histological features of TMJs affected by rheumatoid arthritis, and the detection of secondary amyloidosis and macrophage populations in the TMJs of two patients with progressive rheumatoid arthritis are described.nnnMETHODSnIn two patients (64-year-old man and 61-year-old woman) with rheumatoid arthritis total TMJ replacement were performed. The surgical specimens were studied histologically.nnnRESULTSnIt was found that the articular cartilage had been completely replaced by proliferating fibrous tissue. Congo red staining and polarizing microscopy revealed amyloid deposition in the connective tissue of the joint space. Immunohistochemical staining showed CD 68 positive macrophages around the amyloid deposition in the proliferating soft tissue.nnnCONCLUSIONnTMJ involvement in rheumatoid arthritis followed the same destructive pathway as in other joints. Amyloid deposition and macrophage populations were detected in two TMJs affected by rheumatoid arthritis.

Presence of Human β-Defensin-2 in Oral Lichen Planus and its Histamine Releasing Effect

Abstract Objective: To determine by immunohistochemical means the localization of human β-defensin-2, a peptide with antimicrobial activity, in oral lichen planus. The release of histamine from mast cells elicited by human β-defensin-2 was also investigated. Materials and Methods: Biopsy specimens of oral lichen planus, synthetic human β-defensin-2, human α-defensin-1, and mast cells isolated from Sprague Dawley rats were used. Tissue sections were embedded in paraffin and immunostained by the streptavidin-biotin-coupled peroxidase method. Isolated rat mast cells were injected with synthetic human β-defensin-2 and human α-defensin-1. Evans blue dye was injected into the tail vein of Sprague Dawley rats, followed by various doses of histamine, human β-defensin-2, human α- defensin-1, and saline. Results: Epithelial cells in lichen planus from the corneal layer to the spinous layer, were positively stained with anti-human β-defensin-2 antibody. Mast cells in subepithelial areas were also stained by anti-human β-defensin-2 antibody. Human β-defensin-2-induced histamine release from the isolated rat mast cells occurs in a dose-dependent manner. When human β-defensin-2 was injected into rat skin intradermally, the vascular permeability increased. These responses were completely abolished upon injection of the antihistamine drug diphenhydramine hydrochloride. Conclusion: Human β-defensin-2 and histamine may play an important role in the formation of oral lichen planus.

Histamine Release from Rat Mast Cells Induced by Human α-Defensin-1 Present in Jaw Cyst Fluid

Abstract Objective: To investigate the release of histamine from rat mast cells elicited by human α-defensin-1 contained in jaw cyst fluid. Patients and Methods: Human α-defensin-1 was purified by reversed-phase high-performance liquid chromatography from human jaw cyst fluid, and the mast cells were collected from the peritoneal cavities of rats. Results: Histamine release was induced in isolated rat mast cells by both extracted and synthetic human α-defensin-1. Changes in vascular permeability induced by human α-defensin-1 were also estimated by the passive skin test in rats. Extracted and synthetic human α-defensin-1 induced histamine release from isolated rat mast cells in a dose-dependent manner over a concentration range of 1 to 15 μg/mL; the histamine release induced by the extracted and synthetic human α-defensin-1 (15 μg/mL) was 39.4 ± 2.3 and 37.6 ± 1.8%, respectively. When human α-defensin-1 was injected into rat skin intradermally, the vascular permeability increased. This response occurred with as little as 0.1 μg of human α-defensin-1, and a strong response was observed with 0.5 and 1.0 μg. These responses were completely abolished upon injection with 1 μg of the antihistamine drug diphenhydramine hydrochloride. Conclusion: Human α-defensin-1 in human jaw cyst fluid can act as an inducer of histamine release from mast cells both in vivo and in vitro.