Low-intensity pulsed ultrasound accelerates periodontal wound healing after flap surgery.

BACKGROUND AND OBJECTIVE: A study was conducted to evaluate the effects of low-intensity pulsed ultrasound on wound healing in periodontal tissues after mucoperiosteal flap surgery. MATERIAL AND METHODS: Bony defects were surgically produced bilaterally at the mesial roots of the mandibular fourth premolars in four beagle dogs. The flaps were repositioned to cover the defects and sutured after scaling and planing of the root surface to remove cementum. The affected area in the experimental group was exposed to low-intensity pulsed ultrasound, daily for 20 min, for a period of 4 wk from postoperative day 1 using a probe, 13 mm in diameter. On the control side, no ultrasound was emitted from the probe placed contralaterally. After the experiment, tissue samples were dissected out and fixed in 10% formalin for histological and immunohistochemical analyses. RESULTS: The experimental group showed that the processes in regeneration of both cementum and mandibular bone were accelerated by low-intensity pulsed ultrasound compared with the control group. In addition, the expression level of heat shock protein 70 was higher in the gingival epithelial cells of the low-intensity pulsed ultrasound-treated tooth. CONCLUSION: Our results suggest that osteoblasts, as well as cells in periodontal ligament and gingival epithelium, respond to mechanical stress loaded by low-intensity pulsed ultrasound, and that ultrasound accelerates periodontal wound healing and bone repair.

Aspartate aminotransferase (AST) levels in human periodontium-derived cells.

The ability to objectively assess periodontal disease activity can significantly affect periodontal therapy. Aspartate aminotransferase (AST) is released extracellularly upon tissue destruction which suggests its potential as a key index in a quantitative assay for evaluating periodontal disease activity. The purpose of the present research was to assess the origin of AST in gingival crevicular fluid (GCF) in vitro. An experimental kit was used for the measurement of AST level in human gingival epithelial cells (HGEs), human gingival fibroblasts (HGFs), human periodontal ligament fibroblasts (HPLFs), polymorphonuclear leukocytes (PMNs), and plasma in peripheral blood. AST activity levels were observed in all of the periodontally derived cells, PMNs, and plasma. A significantly high level of AST activity was observed in HGEs (104.93 +/- 8.13 KU/1000 cells). The level of AST activity in HPLFs was 18.09 +/- 3.73 KU/1000 cells. AST activity in PMNs was significantly low, approximately 2% of that observed in HPLFs. These findings may suggest that AST level in GCF is correlated with the destruction of periodontal tissue.

Phagocytic function of salivary PMN after smoking or secondary smoking.

Alterations in polymorphonuclear leukocyte (PMN) functions, such as phagocytosis, chemotaxis, and oxidative burst, play a pivotal role in periodontal pathogenesis. In addition, previous studies have demonstrated a strong relationship between smoking and periodontal disease. In the present study, the effect of cigarette smoking or passive smoking (secondary smoking) on the phagocytic function of salivary PMN (SPMN) was investigated. Twenty volunteers with clinically healthy gingiva (10 smokers, 10 non-smokers) participated in this study. In a small room, the smokers and passive smokers (non-smokers) were instructed to smoke and breathe, respectively, in an identical, specific way for about 4 minutes. SPMN was isolated immediately before and after smoking or passive smoking. PMN was then incubated with fluoresbrite beads for 45 minutes at 37 degrees C and the phagocytic status estimated by using a flow cytometer. Cell viability was determined by trypan blue exclusion (smokers before smoking: 88.3%: smokers after smoking: 89.6%: non-smokers before passive smoking: 89.0%; non-smokers after passive smoking: 89.4%). In both smokers and passive smokers, the proportion of phagocytic cells increased between before and after smoking (smokers before: 33.2%; after: 42.1%: passive smokers before: 36.2%: after: 44.1%). Both increases were statistically significant (P < 0.01). These results demonstrate that the phagocytic activity of SPMN intensifies after smoking and passive smoking. They also suggest that certain substances in cigarette smoke, perhaps nicotine, overstimulate the host response in the oral cavity.

[Biochemical characterization of phenytoin-induced hyperplastic human gingival fibroblasts. Non-collagenous proteins biosynthesis].

Phenytoin (PHT), administered as an anticonvulsant, has a side effect gingiva overgrowth in approximately 50% of patients. The present study was attempted to explore the biochemical mechanism on non-collagenous protein biosynthesis as affected by PHT. Responder cells (RES A3, RES C2) of a patient with gingival overgrowth were obtained by the method of Kawase et al. Normal human gingival fibroblasts (Gin-1), purchased from ATCC, were also used. All cells were inoculated at 1 x 10(4) cells/cm2 (12 multi-well plate or 60 mm tissue culture dish), and then cultured for 4, 8 and 12 days with or without PHT (5 micrograms/ml). Prior to harvesting at the indicated times, cells were incubated with 14C-amino acids (1.25 microCi/ml) for 24 hours. The 14C-labeled proteins were isolated from the cell layers including extracellular matrix, following Kurkinen et al. with a minor change. Each 14C-labeled fraction was dissolved in 3 ml of Aquasol-2 and the radioactivity by a liquid scintillation counter. The DNA content of cell layers affected by PHT was increased on Gin-1, RES A3 and RES C2 at the post-confluence, resulting also in an increase in cell number. Two morphologically different phenotypes of responder cells were observed, differing in nuclear and cell sizes. At 12 days culture, RES A3, were stimulated by PHT, showed increased synthesis of both total extractable proteins (EP) and binding proteins (BP) labeled with 14C-amino acids. Therefore, at least two distinct phenotypic responder cells are present in the PHT-induced overgrowth gingiva, alter the synthesis of non-collagenous proteins.