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Due to increasing incidence of open fracture and increasing application of orthopedic implants, chronic osteomyelitis prevails in recent years, leading to failure of internal fixation, sinus tract formation, long-term abscess discharge and delayed recovery, etc., affecting prognosis and quality of life of the patients, and causing a huge medical and economic burden.The treatment of osteomyelitis has recently progressed from mere debridement to debridement + Masquelet bone reconstruction or osteotomy + llizarov bone transfer which has significantly improved the therapeutic efficacy. However, multiple surgeries, long healing time and massive surgical trauma of the current treatment cause poor compliance in the patients. Therefore, new therapeutic strategies are imperative. Various causes of chronic osteomyelitis involve autoimmunity, inflammatory factors, oxidative stress, local blood supply in osteomyelitis region, drug-resistant bacteria, bacterial virulence and bacterial biofilm which, as an important form of bacteria in the body, has a particularly significant impact on chronic osteomyelitis. Resistance to a variety of eliminating effects by bacteria is achieved mainly by biofilm, including reducing antibiotics concentration, barrier against immune clearance, improving bacterial resistance, spreading bacteria and promoting signal communication between bacteria. Aiming at the key factors and pathways for target research and intervention is the hotspot and trend in the research and treatment of osteomyelitis. Here we review the literature about the role of biofilm in chronic osteomyelitis, which is conducive for further understanding of the biofilm influence on chronic osteomyelitis and related targets, and for prevention and treatment of chronic osteomyelitis as well.
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Objective To investigate the effects of sodium butyrate on the activity of RAW264.7 cells and the osteoclast differentiation.Methods The RAW264.7 cells were treated by sodium butyrate at concentrations of 0,0.25,0.50,1.00,2.00,3.00,4.00 and 5.00 mmol/L,with 3 double pores for each concentration.The cytotoxicity of sodium butyrate on RAW264.7 cells was detected by a CCK-8 kit.The effects of sodium butyrate (0,0.25,0.50 and 1.00 mmol/L) on apoptosis of RAW264.7 cells were detected by Hoechst33342 staining.RAW264.7 cells were induced into osteoclasts by osteoclast differentiation factors.The experiment was carried out in 2 groups (n =3).After induced maturation,the experimental group was treated with 1.00 mmol/L sodium butyrate and the control medium was added only with the same volume of solvent.The number of osteoclasts and the area of bone resorption were observed and compared.The differentiation of RAW264.7 cells was detected by tartrate-resistant acid phosphatase (TRAP) staining.Western blotting was used to detect the effects of sodium butyrate (0,0.25,0.50 and 1.00 mmol/L) on NF-κB-related signaling pathway in RAW264.7 cells.Results Compared with the group of 0 mmol/L sodium butyrate,the activity of cells treated with 1.00,2.00,3.00,4.00 and 5.00 mmol/L sodium butyrate for 24 h was significantly decreased (P ＜ 0.05).Treatment with 1.00 mmol/L sodium butyrate for 24 h induced apoptosis.The number of osteoclasts in the control group and the experimental group were 9.33 ± 2.08 and 4.67 ± 1.16,respectively,showing a significant difference between the 2 groups (t =3.395,P =0.027).The percentages of bone resorption area in the control group and the experimental group were 52.43％ ± 5.38％ and 14.28％ ± 2.72％,respectively,also showing a significant difference between the 2 groups (t =10.970,P ＜ 0.001).Western blot results showed that,compared with other concentrations of sodium butyrate,treatment with 1 mmol/L sodium butyrate on RAW264.7 cells for 24 h led to an increase in the expression levels of cytoplasmic p65,B lymphoma-2 associated X protein and cleaved-caspase 3 and the acetylation of Histone H3 but a decrease in the phosphorylation level of α/β subunit of NF-κB kinase.Conclusions With the increased concentration of sodium butyratecan,the activity of NF-κB may be suppressed and the number of apoptotic cells may increase.1.00 mmol/L sodium butyrate can reduce osteoclast formation and bone resorption area.
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Objective To investigate the clinical features and the correlated reason of upper gastrointestinal bleeding (UGIB) induced by non-steroidal anti-inflammatory drugs (NSAIDs). Methods Five hundred and twenty-eight patients were divided into two groups according to consumption of NSAIDs in the week previous to the onset of bleeding, 116 cases were in NSAIDs group and 412 cases were in non-NSAIDs group. The clinical data was analysed and compared between two groups. Results There was no significant difference in sex, smoking history, and ulcer history between two groups (P> 0.05). The average age was (57.4 ± 12.1) years old and the infection of Hp was 65.5% (76/116) in NSAIDs group, and they were higher than those in non-NSA1Ds group [(44.6 ± 11.9) years old and 25.0% (103/412)](P < 0.01). More gastric ulcer and complex ulcer was seen in NSAIDs group (P <0.01 or <0.05). Conclusion Recognition about the clinical characteristics of NSAIDs relevance UGIB should be strengthened, and side effect of NSAIDs should be reduced as far as possible.
