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Summary Tumor necrosis factor α (10−10–10−8M) had no effects on cyclic AMP production by the osteoblastic osteosarcomal cells, Saos-2 and G292, or normal rat calvarial cells. The cytokine did, however, inhibit the parathyroid hormone (PTH)-induced effect on cyclic AMP in the Saos-2 and normal rat osteoblastic cells. This inhibitory effect did not occur on prostaglandin E2-induced cyclic AMP increases in the osteoblastic cells. Interleukin-1 (10 U/ml −100 U/ml) did not produce any effect on basal levels or PTH-induced cyclic AMP increases in these cells.  相似文献   
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Summary The effects of interleukin-1 (IL-1), forskolin, and tumor necrosis factor (TNF-) on tissue plasminogen activator (t-PA) activity were studied in the human osteoblastic osteosarcoma cell line, G292. t-PA activity was measured in the cell media using the chromogenic substrate, S-2251. After a 24 hour incubation period, IL-1 increased t-PA in a dose-dependent manner. The effect of IL-1 at 10.0 U/ml was partially inhibited in the presence of indomethacin. Forskolin (1.0 M) increased t-PA activity after 24 hours with the effects of combined treatment of IL-1 (1.0 U/ml, 10.0 U/ml) and forskolin being apparently additive in nature. TNF- (10-8–10-7 M) also produced increased t-PA activity in the cell medial after a 24 hour incubation period. These results suggest that the cytokines, IL-1 and TNF-, can increase t-PA activity in G292 cells and that there is both a cAMP-dependent as well as a cAMP-independent pathway involved in the regulation of this osteoblastic cell function.  相似文献   
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Background: The purpose of this retrospective case series study is to identify possible preoperative parameters that could predict postoperative probing depth (PD), clinical attachment level (CAL) gain, or radiographic defect resolution in intrabony defects treated with enamel matrix derivative (EMD). Methods: Sixty‐one chronic periodontitis patients, each contributing a 2‐ or 3‐wall intrabony defect treated with EMD, were included. Clinical parameters recorded included the following: PD; CAL; gingival margin position; supracrestal soft tissue (SST); surgical distances of cemento‐enamel junction (CEJ) to bone crest (CEJ‐BC), CEJ to base of the defect (CEJ‐BD), and BC to BD (BC‐BD); and depth of 2‐ and 3‐wall components. Radiographic parameters recorded included the following: CEJ‐BC, CEJ‐BD, BC‐BD distances, and radiographic defect angle. Postoperative assessments were performed at 12 months. Results: The probability of postoperative PD >4 mm increased 1.6‐fold (odds ratio [OR] = 1.6; 95% confidence interval [CI] = 1.2 to 2.3) with each 1‐mm baseline PD increase. Baseline PD and surgical CEJ‐BD were statistically significant predictors of CAL gain; the greater the baseline PD (OR = 0.5; 95% CI = 0.3 to 0.8) and bone loss (OR = 0.6; 95% CI = 0.3 to 0.9), the less likely that postoperative CAL gain was ≤3 mm. Smoking and SST were significantly associated with defect resolution; failure to achieve ≥65% defect resolution was six‐fold greater for smokers (OR = 6.5; 95% CI = 1.7 to 24.5) and almost double (OR = 1.7; 95% CI = 1.1 to 2.8) for each millimeter of SST increase. Conclusion: In EMD‐treated intrabony defects, baseline PD predicts both CAL gain and postoperative PD. Smoking and SST are predictors of defect resolution.  相似文献   
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Spondyloarthropathy and inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease, are often associated with severe osteopenia/osteoporosis in both children and adults. HLA‐B27 transgenic rats present a phenotype that includes severe colitis and severely accelerated alveolar bone loss. The purpose of this study was to evaluate long bone density status, systemic bone metabolic markers, and intrinsic bone material properties in HLA‐B27 transgenic (TG) rats, and compare them with those of age‐ and sex‐matched wild‐type (WT) animals. The results indicate that in the HLA‐B27 rat, an animal susceptible to both alveolar bone loss (ABL) and long bone osteopenia, there is a statistically significant negative correlation between ABL and long bone bone mineral density (BMD), as well as mineral/matrix ratio at active bone‐forming trabecular surfaces. The TG animals had a lower mineral/matrix ratio and higher relative proteoglycan and advanced glycation end product (?‐N‐Carboxymethyl‐L‐lysine) content and pyridinoline/divalent collagen cross‐link ratio compared with WT. These results may provide better understanding of the interrelationship between osteoporosis and oral bone loss, the underlying causes of the inferior bone strength in the HLA‐B27 transgenic animals, and could prove to be a useful model in the elucidation of the pathophysiology of spondyloarthropathy and IBD‐associated osteopenia/osteoporosis and in the evaluation of pharmacological intervention(s) against such conditions. © 2014 American Society for Bone and Mineral Research.  相似文献   
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Evidence indicates that incisor crown form correlates with clinical periodontal features. It was hypothesized that incisor crown form may explain subject differences in gingivitis expression. The present experimental gingivitis study aimed to assess the effect of incisor crown form on plaque accumulation and gingival inflammation, and on individual susceptibility to plaque-induced gingivitis. Eighty-five periodontally healthy subjects were evaluated. A negative correlation was found between incisor crown width/crown length ratio and bleeding score (p = 0.045). From the 85 subjects, two groups of subjects with either 'long-narrow' or 'short-wide' incisor form were identified. The 'long-narrow' group had a significantly higher bleeding score than the 'short-wide' group (p = 0.014). No significant differences were found in the incisor crown width/crown length ratio between previously identified 'high responder' and 'low responder' subjects (Trombelli et al., 2004a). In conclusion, incisor crown form appears to affect the bleeding response of inflamed gingival tissues, while it exerts no influence on explaining differences in individuals' susceptibility to plaque-induced gingivitis.  相似文献   
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BACKGROUND: HLA-B27 transgenic rats exhibit generalized, severe inflammatory reactions and spontaneously develop arthritis and chronic gastrointestinal inflammation, as well as inflammatory lesions in other tissues. Our hypothesis was that HLA-B27 rats would also be susceptible to inflammatory periodontal disease, and therefore alveolar bone loss. The purpose of this investigation was to compare the naturally occurring alveolar bone loss in HLA-B27 and wild type rats. METHODS: Age- and sex-matched HLA-B27 transgenic (TG) and wild type Fischer 344 (WT) female retired breeders, and their age-matched male WT breeding mates, were examined for alveolar bone loss (ABL). Thirty-eight animals were used: twelve, 20, and 6 animals were 6, 8, and 12 months old, respectively. ABL was measured as the exposed root surface area (mm2) in the defleshed maxilla and mandible. RESULTS: The coefficient of variation for replicate ABL measurements was 4.4%. For the 6- and 8-month age groups, ABL was significantly greater in TG rats compared to WT rats. The observed difference in ABL between TG and WT animals did not reach statistical significance for the 12-month age group. Within each of the two animal groups (TG and WT), ABL was significantly different between age groups. The ABL rate of TG female rats was 42% to 250% greater than that of WT female rats, depending on the age range examined. CONCLUSIONS: HLA-B27 rats are susceptible to accelerated alveolar bone loss and could serve as an animal model of alveolar bone loss pathogenesis.  相似文献   
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