Bite force, occlusal contact area and masticatory efficiency before and after orthognathic surgical correction of mandibular prognathism.

The purpose of this study was to evaluate bite force, occlusal contact area and masticatory efficiency before and after sagittal split ramus osteotomy in 27 patients with mandibular prognathism, in comparison with 27 control subjects with normal occlusion. Bite force and occlusal contact area were simultaneously measured with a computerized occlusal analysis system, the Dental Prescale system. Masticatory efficiency was estimated by a low-adhesive colour-developing chewing-gum system. The data were collected at initial medical consultation, immediately before surgery, and at 6 weeks, 3 months, 6 months, 1 year and more than 2 years after surgery. Both bite force and occlusal contact area of the patients before surgery were significantly less than those of the controls. Although all three parameters had improved after orthognathic surgery, the bite force and occlusal contact area did not reach the values of the controls within 2 years postoperatively; masticatory efficiency at 2 years after surgery drew near to control levels. Bite force correlated with occlusal contact area in the patients postoperatively, whereas masticatory efficiency did not correlate with either of the other two parameters. These results suggest that further adjustment of occlusion and mechanical advantage should be considered before the end of treatment.

Hypercalcemic complication in patients with oral squamous cell carcinoma.

Hypercalcemia is one of the metabolic complications associated with cancer. To assess the frequency of hypercalcemia in patients with squamous cell carcinoma (SCC), 242 patients who were evaluated as having SCC in the oral cavity between July 1995 and June 2001 were investigated. All patients were periodically monitored for their serum level of calcium (Ca). Hypercalcemia was defined as a serum Ca concentration higher than 11 mg/dl. By this definition, hypercalcemia was detected in 12 of the 242 patients (5.0%). All 12 patients were at an advanced stage of oral SCC. In these 12 patients, the serum level of parathyroid hormone-related protein (PTH-rP) was also significantly elevated. Therefore, we diagnosed these diseases as humoral hypercalcemia of malignancy (HHM). Moreover, we studied the efficacy of anti-hypercalcemic therapy on the quality of life (QOL). The European Organization for Research and Treatment of Cancer (EORTC) QLQ-C30 was used for estimation of QOL. The patients with HHM who were administrated drugs such as bisphosphonate and calcitonin showed a reduction in their Ca and PTH-rP levels, and the six of ten EORTC QLQ-C30 subscales (emotional functioning, cognitive functioning, fatigue, dyspnoea, nausea/vomiting and appetite loss) were also improved after the anti-hypercalcemic therapy. However, these suppressive effects were temporary. The median survival time after the diagnosis of HHM was only 54.9+/-18.3 days (range 27-86 days). Therefore, HHM in SCC appears to be an ominous prognostic sign. Although anti-hypercalcemic therapy has a palliative role, the patients may be in less discomfort during the terminal stage of their illness.

Role of interleukin-8 secreted from human oral squamous cell carcinoma cell lines.

Interleukin-8 (IL-8) is an important cytokine involved in tumor growth and angiogenesis in a variety of malignancies. Furthermore, matrix metalloptoteinases (MMPs) also play important roles in the invasion and metastasis of carcinomas including oral squamous cell carcinoma (OSCC). We studied whether IL-8 and MMPs participate in tumorigenesis and metastasis of OSCC. First, we investigated the gene and protein expressions of IL-8 and IL-8 receptor (IL-8R), and the effect of IL-8 on proliferation, migration and invasion of OSCC. Second, we thus also investigated the effect of IL-8 on MMP release in OSCC cells. OSCC cell lines NA and HSC-4 constitutively expressed IL-8 mRNA and secreted its protein in vitro. The production of IL-8 was significantly enhanced by the addition of tumor necrosis factor (TNF)-alpha and IL-beta, but not interferon (IFN)-gamma, granulocyte-macrophage colony-stimulating factor (GM-CSF) or IL-2. Flow cytometric analysis revealed the constitutive expression of both receptors of IL-8, IL-8RA and IL-8RB, in OSCC cell lines. The expression of IL-8 receptors in HSC-4 cells was stronger than that in NA cells. The intensity of IL-8RA expression was stronger than that of IL-8RB expression in each cell line. The expression of IL-8 receptors was not altered by the addition of cytokines such as TNF-alpha and IL-1beta. The conditioned medium containing IL-8 from OSCC cell lines induced migration and invasion of OSCC cells, but did not change cell proliferation. The differences in migrational and invasive ability between NA cells and HSC-4 cells were correlated with the expression intensity of IL-8 receptors in each cell line. Neutralizing antibodies to IL-8, IL-8RA and IL-8RB partially inhibited the chemotactic activity induced by conditioned medium. The expression of MMP-2, -7 and -9 was detected in culture supernatants from these OSCC cell lines. The expressions of MMP-7 protein and mRNA were enhanced by the addition of rIL-8, but that of other MMPs was not observed in a similar manner. These results suggest that IL-8 secreted from OSCC may contribute to the invasion of OSCC through the regulation of MMP-7 expression.

Inhibitor of cyclooxygenase-2 induces cell-cycle arrest in the epithelial cancer cell line via up-regulation of cyclin dependent kinase inhibitor p21.

Cyclooxygenase-2 is the rate-limiting enzyme in synthesis of prostaglandins and other eicosanoids. Prior reports have shown that inhibition of cyclooxygenase-2 activity, either by selective inhibitors or by antisense oligonucleotide, results in suppression of growth of squamous cell carcinoma cell lines which express high cyclooxygenase-2 levels, such as NA, a cell line established from a squamous cell carcinoma of the tongue. To investigate the mechanisms by which cyclooxygenase-2 inhibitors suppressed growth of these cells, the effects of NS-398, the selective cyclooxygenase-2 inhibitor, on cell-cycle distribution were examined. NS-398 induced G0/G1 cell-cycle arrest in NA cells which expressed cyclooxygenase-2. G0/G1 arrest induced by NS-398 was accompanied by up-regulation of cyclin-dependent kinase inhibitor p21, but not by up-regulation of the other cyclin-dependent kinase inhibitors. Transfection with p21 antisense oligonucleotide inhibited cell-cycle arrest induced by NS-398. Accumulation in G0/G1 was also observed in NA cells transfected with cyclooxygenase-2 antisense oligonucleotide. On the other hand, NS-398-treated NA cells showed a loss of plasma membrane asymmetry, a marker of early events in apoptosis. However, NS-398 did not induce other morphological and biochemical changes related to apoptotic cell death. These results suggest that cyclooxygenase-2 inhibitor induces G0/G1 cell-cycle arrest in NA cells by up-regulation of p21. Our results also suggest that NS-398 is not sufficient to complete the whole process of apoptosis in NA cells, although it induces an early event in apoptosis.

Hypercalcemia in patients with oral squamous cell carcinoma.

Humoral hypercalcemia of malignancy (HHM) is one of the most common metabolic complications associated with cancer. A retrospective study of hypercalcemia in patients with squamous cell carcinoma of the oral cavity was undertaken. All patients were periodically monitored for their serum level of calcium (Ca). Hypercalcemia was defined as a serum Ca concentration higher than 11 mg/dl of the correction for serum albumin concentration. The serum levels of parathyroid hormone related protein (PTH-rP) were also measured by radioimmunoassay. Hypercalcemia was detected in ten of 246 patients (4.1%). All ten patients were at an advanced stage of oral squamous cell carcinoma (SCC, Stage IVA, IVB or IVC). In these ten patients, the serum level of PTH-rP was significantly elevated, 238 +/- 91 pmol/l (range, 108-380 pmol/L). The patients with HHM who underwent antihypercalcemic therapy showed reduced Ca levels relating to PTH-rP levels; however, the Ca concentration was temporarily improved after anti-hypercalcemic treatment. The median survival time after diagnosis of HHM was only 55.8 +/- 19.9 days (range, 27-86 days). HHM in oral cancer is likely attributable to PTH-rP, and its occurrence appears to be an ominous prognostic sign.

Inhibitors of cyclooxygenase-2 (COX-2) suppressed the proliferation and differentiation of human leukaemia cell lines.

Prostaglandins (PG) are known to play important roles in the proliferation and differentiation of leukaemia cells. The effect of the inhibitors of cyclooxygenase-2 (COX-2), a rate-limiting enzyme for the synthesis of PG, on the proliferation and differentiation of leukaemia cell lines was investigated. COX-2 inhibitors, NS-398 and nabumetone, suppressed the proliferation of U-937 and ML-1 cells by inducing a G0/G1 cell-cycle arrest. Cell-cycle arrest induced by these COX-2 inhibitors was not associated with an upregulation of the cyclin-dependent kinase inhibitors. COX-2 inhibitors also inhibited the differentiation of these cells induced by interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and retinoic acid (RA). Treatment with NS-398 did not suppress the levels of PGs produced by these cells. Although COX-2 antisense oligonucleotide showed a similar inhibitory effect on these cells, its inhibitory effect was smaller than that of NS-398. These results suggest that COX-2 inhibitors may suppress the proliferation and differentiation of leukaemia cells both via COX-2-dependent and -independent pathways.

Specific inhibition of cyclooxygenase-2 results in inhibition of proliferation of oral cancer cell lines via suppression of prostaglandin E2 production.

Prostaglandins (PGs) are known to play important roles in the proliferation of various types of cancer cells. PGs are produced by the action of cyclooxygenase (COX) enzymes, and two forms of COX, COX-1 and COX-2, have been described. Previous studies have demonstrated that overexpression of COX-2 is associated with colon carcinogenesis, tumor invasion and metastatic potential of colon cancer. In this study, the role of COX-2 on proliferation of squamous cell carcinoma cell lines was investigated. NS-398, a selective COX-2 inhibitor, inhibited proliferation of NA cells, a squamous cell caricinoma cell line that constitutively expresses COX-2 mRNA. NS-398 suppressed the spontaneous production of PGE2 by NA cells, and the antiproliferative effect of NS-398 was abolished by addition of PGE2. Similar results were obtained from experiments using COX-2 antisense oligonucleotide. These results suggest that specific inhibition of COX-2 inhibits proliferation of cancer cells expressing COX-2 mRNA via suppression of PGE2 production.

Involvement of caspases in 5-FU induced apoptosis in an oral cancer cell line.

Although many anticancer drugs have been reported to induce apoptosis in cancer cells, the underlying mechanism remains unclear (1-3). Recent studies have revealed that the caspase family of cysteine proteases have been shown to play an important role in the regulation of several apoptotic processes. Thus, the present study investigated whether apoptosis induced by anticancer drugs is mediated by the activation of caspase cascade. NA cells, a squamous cell carcinoma cell line, were exposed to cisplatin (CDDP) or 5-fluorouracil (5-FU) with or without inhibitors of caspase 1, 3 and 8. Analysis of DNA fragmentation revealed that caspase inhibitors consistently inhibited DNA fragmentation induced by 5-FU. During the early stages of apoptosis, phosphatidylserine (PS) is translocated from the inner side of the plasma membrane to the cell surface. This PS externalization was markedly inhibited by treatment with caspase-8 inhibitor. These findings suggested that 5-FU induced apoptosis was mediated by the activation of a caspase cascade involving caspase 1, 3 and 8.

Effects of cytokines on the production of nitric oxide in a chondrogenic cell line established from human osteogenic sarcoma.

OBJECTIVES: The purpose of this study was to examine the effects of various cytokines and/or lipopolysaccharide (LPS) on nitric oxide (NO) production from USAC, a newly established clonal cell line derived from human osteogenic sarcoma that expressed chondrocytic phenotypes. MATERIALS AND METHODS: No production was measured by Griess method. Inducible nitric oxide synthase (iNOS) mRNA was detected by PCR analysis. Western blotting analysis and immunocytochemistry was used to detect iNOS protein. RESULTS: Although USAC cells treated without any stimulants produced only small amounts of NO, exposure to cytokines and/or LPS induced iNOS in USAC cells and produced high levels of NO. The stimulatory effects of cytokines and/or LPS on NO production required TNF-alpha. TNF-alpha alone neither induced iNOS in USAC cells nor caused production of NO, but addition of TNF-alpha to USAC cells pretreated with LPS and IFN-gamma enhanced the expression of iNOS mRNA, induced iNOS protein and produced NO. Dexamethasone inhibited the stimulatory effect of TNF-alpha. CONCLUSIONS: The responsiveness of USAC cells to cytokines and/or LPS and steroid hormone on NO production was quite different from that reported for rabbit and human articular cartilaginous cells. The differences in responsiveness between articular cartilaginous chondrocytes and USAC cells might have been because USAC cells were established from a malignant tumor.

Establishment of a cell line with phenotypes of chondrocyte from a human osteogenic sarcoma of the mandible.

We have succeeded in transplanting a human osteogenic sarcoma of the mandible into athymic mice. The transplanted tumor showed marked chondrogenesis and mineralization. Recently, a cell line (USAC) with phenotypes of chondrocyte has been established from the transplanted tumor. USAC cells were stellate or spindle-shaped in sparse culture, but polygonal or spherical at sub-confluency to confluency. In long-term culture, the cells were condensed and calcified nodules were formed. Production of types I, II and X collagen were detected by immunohistochemical staining and Western blot analysis. Type I collagen was strongly expressed in the stellate or spindle-shaped cells. Although type II collagen was usually present in all cells during culture, it was strongly stained in polygonal cells at confluency. Type X collagen was seen in large polygonal cells around calcified nodules. Marked [35S]-sulfate uptake and metachromasia were seen at the confluent stage and in the nodule. The cells around the nodules were positive for alkaline phosphatase, and the center of the nodules was stained with alizarin red. The potentiality of cartilage formation was confirmed by in vivo experiments using a diffusion chamber in athymic mice. These observations indicate that USAC cells maintain characteristics of chondrocyte progenitor cells and thus may serve as a useful model to study the sequential events of chondrogenesis and the process of morbid endochondral calcification. This experiment also demonstrated that transplantation of tumor tissue into athymic mice is a convenient strategy for establishment of a cell line.

Changes in susceptibility to Fas-mediated apoptosis during differentiation of HL-60 cells.

The Fas-mediated pathway has been implicated as an important cellular pathway mediating apoptosis in diverse cell types. We conducted studies to examine the susceptibility to Fas-mediated apoptosis of HL-60 cells treated with differentiation-inducing factors such as dimethyl sulfoxide (DMSO), retinoic acid (RA), and 1alpha, 25 dihydroxyvitamin D3 (VD3). Although the expression of Fas antigen (Ag) and its mRNA showed a marked increase in HL-60 cells with cell differentiation, that of Bcl-2 protein and its mRNA revealed the reverse. The expression of caspase proteins such as caspases-3 and -8 was also enhanced during cell differentiation. DNA fragmentation, annexin V binding, and caspase activities increased in differentiated HL-60 cells with the addition of anti-Fas Ag antibody. These findings were more clearly demonstrated in DMSO- or RA-induced neutrophil-like cells than in VD3-induced monocyte-like cells. Therefore, susceptibility to Fas-mediated apoptosis showed an increase with differentiation of HL-60 cells, especially in the neutrophil lineage. These results suggest that the difference of susceptibility to Fas-mediated apoptosis among cell populations depends on the expression of Fas Ag, Bcl-2, and caspases. Cell maturation and susceptibility to Fas-mediated apoptosis may be linked in hematopoietic cells.

Proliferation and differentiation of bone marrow cells on titanium plates treated with a wire-type electrical discharge machine.

For successful dental implants, it is necessary to obtain satisfactory osteointegration at the site of both the cortical and trabecular bones in the jaw. Bone marrow stromal cells differentiate into osteoblast-lineage cells and have an important role in bone remodeling. In this experiment, the responsiveness of bone marrow cells to a titanium plate with a rough surface was compared with that of a titanium plate with a smooth surface. The rough surface was created by treating with a wire-type electrical discharge machine, and the smooth plate was produced by polishing with 1.500-grade emery paper. The results indicated that, though bone marrow cells proliferated on both plates, the proliferation pattern and cell growing time on the plates were different. While the cells on the smooth plate proliferated along the grooves produced by polishing, the cells on the rough plate proliferated randomly and more rapidly. As bone marrow cells consisted of heterogeneous cell populations involving hematopoietic cells, we collected bone marrow mesenchymal stromal cells that proliferated on plastic dishes and studied the proliferation and differentiation of these cells. Stromal cells on the rough plate more actively proliferated than those on the smooth plate. In long-term culture, the cells on the rough plate showed higher alkaline phosphatase activity and produced cell nodules. The cells on the smooth plate were stripped off the plate without nodule formation. These results indicated that bone marrow stromal cells on the rough plate could more rapidly proliferate and differentiate into osteoblast-lineage cells compared with those on the smooth plate.

Recombinant human bone morphogenetic protein-2 stimulates osteoblastic differentiation in cells isolated from human periodontal ligament.

Periodontal ligament cells may play an important role in the successful regeneration of the periodontium. We investigated the effects of recombinant human bone morphogenetic protein-2 (rhBMP-2), one of the most potent growth factors that stimulates osteoblast differentiation and bone formation, on cell growth and osteoblastic differentiation in human periodontal ligament cells (HPLC) isolated from four adult patients. rhBMP-2 induced no significant changes in cell growth in any of the HPLCs. rhBMP-2 at concentrations over 50 ng/mL significantly stimulated alkaline phosphatase (ALPase) activity and parathyroid hormone (PTH)-dependent 3', 5'-cyclic adenosine monophosphate accumulation, which are early markers of osteoblast differentiation, in the HPLCs. rhBMP-2 (500 ng/mL) also slightly enhanced the level of PTH/PTH-related peptide receptor mRNA expression in these cells. While interleukin-1 beta enhanced ALPase activity stimulated with rhBMP-2, tumor necrosis factor-alpha inhibited the rhBMP-2-stimulated activity. Interleukin-6 induced no significant changes in ALPase activity stimulated with rhBMP-2. Although HPLCs, whether treated with rhBMP-2 or not, could not produce measurable amounts of osteocalcin, which is a marker of more mature osteoblasts, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] induced osteocalcin mRNA expression and protein synthesis in these cells. rhBMP-2 inhibited 1,25(OH)2D3-induced osteocalcin synthesis in HPLCs at both the mRNA and protein levels. These results suggest that rhBMP-2 provides an anabolic effect on periodontal regeneration by stimulation of osteoblastic differentiation in human periodontal ligament cells, and that this stimulatory effect is differentially modulated by inflammatory cytokines during the course of periodontal regeneration.

Redo cardiac surgery for atrial septal defect in a patient with idiopathic thrombocytopenic purpura. Preoperative management with high-dose intravenous gamma-globulin.

A 58-year-old woman with idiopathic thrombocytopenic purpura required redo cardiac surgery of atrial septal defect closure, mitral annuloplasty, and tricuspid annuloplasty. Preoperative high-dose intravenous gamma-globulin and platelet transfusion after termination of cardiopulmonary bypass allowed successful redo cardiac surgery. Management of a patient with idiopathic thrombocytopenic purpura undergoing open heart surgery are discussed.

Elevated production of salivary nitric oxide in oral mucosal diseases.

Nitric oxide (NO) is known to play an important role in biological systems. In this study, we measured levels of NO in the saliva of 39 patients with oral mucosal diseases: 21 had oral lichen planus (OLP) and 18 had recurrent aphthous ulceration (RAU). NO was assayed using the Griess reagent, which measures nitrite (NO2), the byproduct of NO. NO2 was detected in all tested samples, and levels in the saliva of patients were significantly increased relative to those of healthy subjects. We also examined the effect of NO on fibroblasts, keratinocytes and NA cells (an epithelial cancer cell line) in vitro. S-nitroso-N-acetyl-DL-penicillamine (SNAP) and 3-morpholinosydnonimine (SIN-1) were used as NO donating reagents. The results revealed that cell viability was significantly reduced by NO derived from SNAP and SIN-1 in a dose-dependent manner. Although the role of salivary NO in normal physiology is as yet unknown, these findings suggest that excessive salivary NO plays a potential role in modifying oral mucosal diseases as a physiopathological regulator.

Altered growth response of oral mucosal keratinocytes in p53-deficient mice.

P53 has important regulatory functions in cell growth, differentiation and apoptosis. Here we analyzed the effects of p53 on the growth response of oral mucosal keratinocytes (OMKCs) using p53-deficient (p53-/-) mice. No morphological difference was found between p53-/- and wild-type (p53+/+) oral mucosa. In a long-term culture, p53-/- OMKCs continued to proliferate past the point at which p53+/+ became senescent. The percentage of p53-/- OMKCs in the G0/G1 phase was lower than that of p53+/+ OMKCs. Proliferation of cultured OMKCs induced by epidermal growth factor (EGF) and interleukin-(IL)-1alpha was more strongly enhanced in p53-/- than in p53+/+ mice. Such an enhanced response was not due to increased mRNA expression of growth factor receptors. These data suggest that p53 acts as a modulator of G1 arrest in OMKCs and is also involved in the regulation of responses to EGF and IL-1alpha without affecting the expression of their receptors.

Synergistic induction of ICAM-1 expression by cisplatin and 5-fluorouracil in a cancer cell line via a NF-kappaB independent pathway.

Cisplatin (CDDP) and 5-fluorouracil (5-FU) are common anti-tumour agents, and the anti-tumour effect of CDDP and 5-FU are synergistically enhanced by combined treatment. To clarify the mechanisms of this synergism, we examined the effect of CDDP and 5-FU on the expression of cell adhesion molecules involved in recognition of cancer cells by T lymphocytes. When NA cells, a squamous cell carcinoma cell line, were exposed to CDDP and 5-FU for 18 h, the expression of intercellular adhesion molecule-1 (ICAM-1) was synergistically induced, whereas CDDP or 5-FU alone did not induce the expression of ICAM-1, as determined by flow cytometry. Expression of ICAM-2 and ICAM-3, which are recognized by the same counter receptor on T-cells, were not up-regulated by CDDP and 5-FU. RT-PCR analysis showed that the induction of ICAM-1 on NA cells might be due to transcriptional induction of ICAM-1 mRNA. Treatment with genistein, a protein tyrosine kinase (PTK) inhibitor, inhibited the induction of ICAM-1 on NA cells by CDDP and 5-FU, whereas staurosporin, a protein kinase C inhibitor, did not. Although CDDP and 5-FU induced binding at the nuclear factor kappa B (NF-kappaB) site in the ICAM-1 promoter, pretreatment with genistein did not prevent CDDP and 5-FU-induced binding at the NF-kappaB site. Moreover, a NF-kappaB nuclear translocation inhibitor did not inhibit the induction of ICAM-1 expression by treatment with CDDP and 5-FU. The synergistic effect of CDDP and 5-FU was not specific to NA cells, since ICAM-1 was synergistically induced by CDDP and 5-FU on HSC-4 cells, a squamous cell carcinoma cell line. These findings indicate that treatment with CDDP and 5-FU induces ICAM-1 expression by a NF-kappaB independent regulatory mechanism involving PTK.

Nitric oxide up-regulates the expression of intercellular adhesion molecule-1 on cancer cells.

Nitric oxide (NO) is an unstable free radical that functions as a cytotoxic agent secreted by macrophages to kill cancer cells. Here we report the effect of NO on the expression of intercellular adhesion molecule-1 (ICAM-1) on cancer cells. NO donors such as SNP, SNAP and SIN-1 up-regulated the expression of ICAM-1 on NA cells, a squamous cell carcinoma cell line. Northern blot analysis showed that the induction of ICAM-1 might be due to transcriptional induction of ICAM-1 mRNA. Up-regulation of ICAM-1 mRNA by NO donors was inhibited by carboxy-PTIO, a NO scavenger. Although NF-kappaB activity was induced by NO donors, AP-1 was not induced by them. Staurosporin, a protein kinase C (PKC) inhibitor, inhibited the induction of ICAM-1 on NA cells by NO, whereas genistein, a protein tyrosine kinase inhibitor, did not. These findings indicate that NO up-regulates ICAM-1 expression on cancer cells by a regulatory mechanism involving PKC and suggest that NF-kappaB, but not AP-1, might be involved in induction of ICAM-1 by NO in cancer cells.

Changes in bite force and occlusal contacts in patients treated for mandibular prognathism by orthognathic surgery.

PURPOSE: The purpose of this study was to evaluate changes in bite force and occlusal contacts before and after orthognathic surgery in patients with mandibular prognathism and to compare the findings with those in controls with normal occlusion. PATIENTS AND METHODS: Bite force and occlusal contacts were analyzed in 23 (7 male and 16 female) patients with mandibular prognathism before and after sagittal split ramus osteotomy, and in 20 (10 male and 10 female) controls with normal occlusion. The bite force and occlusal contacts were simultaneously measured by a computerized occlusal analysis system, the T-Scan system, immediately before surgery, and at 6 weeks, 3 months, 6 months, and 1 year postoperatively. RESULTS: Both the bite force and occlusal contacts in the patients were significantly less than those in the controls before surgery. Although both the bite force and occlusal contacts in the patients were improved by the orthognathic surgery, neither approached the level in the controls within 1 year. Bite force was correlated with the number of occlusal contacts in both patient and control groups. CONCLUSION: The postoperative masticatory function does not reach control levels even 1 year after the orthognathic surgery for mandibular prognathism. Therefore, further adjustment of the occlusion should be considered before the end of treatment.