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Fluorine is an important element widely present in nature, and moderate intake can prevent dental caries and promote bone development. However, long-term excessive intake can lead to fluorosis, damaging tissues or organs such as teeth, bones, heart muscle, and blood vessels. Bone marrow mesenchymal stem cells (BMSCs) play an important role in the repair process of bone injury due to their excellent multi-directional differentiation potential. Therefore, studying BMSCs is of great value in the treatment of fluorosis caused by fluoride poisoning. This article summarize the progress on the effect of fluoride on BMSCs, providing new ideas for the study of the pathogenesis and clinical treatment of fluorosis.
ABSTRACT
Objective:To explore the changes of mitophagy- and apoptosis-related protein expressions after spinal cord injury in rats and its related mechanism.Methods:Ninety-six healthy female SD rats were divided into sham surgery group ( n=48) and spinal cord injury group ( n=48) according to the random number table. Each group was divided into six time points of 1, 3, 7, 14, 21 and 28 days with 8 rats at each time point. In the sham surgery group, the T 8-9 spinous processes and vertebral plates were removed without damage to the spinal cord; in the spinal cord injury group, the spinal cord injury model was established using Allen′s method. At each post-injury time point in two groups, BBB score was used to evaluate the motor function of the rats; HE staining was used to observe the histopathological changes of the spinal cord; immunofluorescence was used to observe the co-localized positive cells of the voltage-dependent anion channel protein 1 (VDAC1) with microtubule-associated protein 1 light chain 3 (LC3) II, E3 ubiquitin ligase (Parkin), and polyubiquitin-binding protein (p62); Western blotting was used to observe expressions of the mitochondrial LC3 II/LC3 I, cytoplasmic Parkin, mitochondrial Parkin, cytoplasmic p62, mitochondrial p62, cytoplasmic apoptotic proteins (Bax), mitochondrial Bax, cytoplasmic cytochrome C (Cyt C), and mitochondrial Cyt C. Results:(1) Compared with the sham surgery group [(21.00±0.00)points at all time points], the BBB scores in the spinal cord injury group were (0.94±0.50)points, (1.69±0.70)points, (4.13±0.99)points, (11.81±1.03)points, (15.06±1.12)points and (18.38±0.83)points at 1, 3, 7, 14, 21 and 28 days after injury, respectively ( P<0.01). (2) Compared with the sham surgery group, the structure in the spinal cord injury group was significantly disrupted at 1 and 3 days after injury, when a large number of hemorrhagic foci, inflammatory cell infiltration, neuronal swelling, and cavity formation were observed. At 7 and 14 days after injury, the number of hemorrhagic foci was markedly reduced compared with the earlier period, when swollen neuronal cytosols, inflammatory cell infiltration and a large number of cavities were found. At 21 and 28 days after injury, a large number of cells were seen to be involved in the repair and the arrangement of cells was disorganized. (3) Compared with the sham surgery group, the number of co-localized positive cells of VDAC1 with LC3 II, Parkin and p62 separately in the spinal cord injury group, markedly increased at 1 and 3 days after surgery, and gradually decreased after that. (4) In the sham surgery group and at 1, 3, 7, 14, 21 and 28 days after injury in the spinal cord injury group, the mitochondrial LC3 II/LC3 I expression levels were 0.56±0.05, 1.00±0.05, 1.19±0.11, 0.86±0.05, 0.80±0.08, 0.66±0.13 and 0.51±0.11, respectively; the cytoplasmic Parkin expression levels were 0.80±0.13, 0.47±0.08, 0.29±0.06, 0.57±0.07, 0.70±0.05, 0.97±0.09 and 0.88±0.12, respectively; the mitochondrial Parkin expression levels were 0.67±0.09, 1.07±0.18, 1.27±0.15, 0.82±0.12, 0.59±0.09, 0.53±0.13 and 0.57±0.14, respectively; the cytoplasmic p62 expression levels were 1.25±0.08, 1.04±0.04, 0.94±0.05, 1.09±0.05, 1.19±0.06, 1.20±0.04 and 1.27±0.05, respectively; the mitochondrial p62 expression levels were 0.61±0.06, 0.88±0.07, 1.09±0.09, 0.98±0.07, 0.70±0.08, 0.68±0.08 and 0.60±0.09, respectively; the cytoplasmic Bax expression levels were 0.92±0.08, 0.67±0.07, 0.36±0.08, 0.48±0.08, 0.69±0.06, 0.88±0.11 and 0.94±0.08, respectively; the mitochondrial Bax expression levels were 0.57±0.04, 0.74±0.04, 0.91±0.05, 0.76±0.05, 0.63±0.08, 0.61±0.05 and 0.57±0.05, respectively; the cytoplasmic Cyt C expression levels were 0.28±0.05, 0.81±0.07, 1.12±0.08, 0.64±0.07, 0.67±0.13, 0.60±0.11 and 0.37±0.06, respectively; and the mitochondrial Cyt C expression levels were 1.02±0.07, 0.91±0.14, 0.37±0.07, 0.73±0.06, 0.91±0.11, 0.95±0.13 and 1.10±0.15, respectively. Compared with the sham surgery group, in the spinal cord injury group mitochondrial LC3II/LC3I had the highest expression level at 3 days after injury; cytoplasmic Parkin had the lowest expression level at 3 days after injury; mitochondrial Parkin had the highest expression level at 3 days after injury; cytoplasmic p62 had the lowest expression level at 3 days after injury; mitochondrial p62 had the highest expression level at 3 days after injury; cytoplasmic Bax had the lowest expression level at 3 days after injury; mitochondrial Bax had the highest expression level at 3 days after injury; cytoplasmic Cyt C had the highest expression level at 3 days after injury; and mitochondrial Cyt C had the lowest expression level at 3 days after injury. Conclusion:Mitochondrial autophagy and apoptosis are enhanced after spinal cord injury in rats, and the potential mechanism may be associated with the transfer of Parkin and P62 from the cytoplasm to the damaged mitochondria for enhanced mitophagy and the release of a large amount of Cyt C from the mitochondria caused by the transfer of Bax from the cytoplasm to the damaged mitochondria for enhanced apoptosis.
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Osteoporotic vertebral compression fracture (OVCF) can lead to lower back pain and may be even accompanied by scoliosis, neurological dysfunction and other complications, which will affect the daily activities and life quality of patients. Vertebral augmentation is an effective treatment method for OVCF, but it cannot correct unbalance of bone metabolism or improve the osteoporotic status, causing complications like lower back pain, limited spinal activities and vertebral refracture. The post-operative systematic and standardized rehabilitation treatments can improve curative effect and therapeutic efficacy of anti-osteoporosis, reduce risk of vertebral refracture, increase patient compliance and improve quality of life. Since there still lack relevant clinical treatment guidelines for postoperative rehabilitation treatments following vertebral augmentation for OVCF, the current treatments are varied with uneven therapeutic effect. In order to standardize the postoperative rehabilitation treatment, the Spine Trauma Group of the Orthopedic Branch of Chinese Medical Doctor Association organized relevant experts to refer to relevant literature and develop the "Guideline for postoperative rehabilitation treatment following vertebral augmentation for osteoporotic vertebral compression fracture (2022 version)" based on the clinical guidelines published by the American Academy of Orthopedic Surgeons (AAOS) as well as on the principles of scientificity, practicality and advancement. The guideline provided evidence-based recommendations on 10 important issues related to postoperative rehabilitation treatments of OVCF.
ABSTRACT
Fluorosis is an endemic disease caused by prolonged exposure to excessive fluoride and is considered a serious public health problem in many countries. In recent years, the damage of chronic fluorosis to the central nervous system has attracted extensive attention from scholars at home and abroad. The mechanisms of neurotoxicity caused by fluorosis include oxidative stress, inflammatory reaction, autophagy, neurotransmitters and related enzymes, changes in neural signaling pathways, abnormal neuronal energy metabolism of neurons, cell apoptosis, etc., causing permanent damage to human brain structure, impaired learning ability, memory dysfunction and behavioral problems. This article reviews the effects of fluorosis on the nervous system and related mechanisms, and provides a reliable basis for prevention and treatment of fluorosis.
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[Objective]To summarize results of treating complex proximal tibia fractures with less invasive stabilization system(LISS),and to explore the concept and technology of LISS.[Method]From January 2004 to March 2006,39 cases of complex proximal tibia fractures were treated with less invasive stabilization system,including 26 male and 13 female.The mean age of the patients was 34.8 years(range 22 to 54 years).According to the AO/OTA fracture classification,there were 19 cases in type 41-A3,12 cases in type 41-C2,4 cases in type 41-C3,4 cases in proximal type 42.Seven cases were open fractures and were classified as 3 grade Ⅰ,4 grade Ⅱ open fracture according to the system of Gustilo.Eleven patients were multitraumatic patients.[Result]All the cases were followed up for averaging 15.6 months(10～21 months).The mean operation time was 75 min(60～130 min).All fractures healed,the averaging healing time was 13 weeks(11～16weeks).The averaging blood lost was 300 ml(170～500 ml).The postoperative alignment of 33 fractures was satisfactory,5 cases had 6?～ 8 ?valgus auglation,one case had 5?varus auglation in coronal plane.The mean time of weight bearing was 14.2 weeks(11～18 weeks).The range of movement was 100?～120?.All the cases had no infection,breakage of screws and plates,failed fixation and so on.According to HSS scores system,there were 26 excellent cases,7 good cases,5 fair cases,1 poor case,the excellent and good rate was 84.6%.[Conclusion]Less invasive stabilization system,providing stable fixation and optimizing early bone union and functional rehabilitation,is a realistic therapy in treatment of complex proximal tibia fractures.Exact comprehension of LISS concept and procedure,adjustment according to cases,are very important to assure satisfactory results.