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From the perspective of the physiological basis of liver and kidney sharing the common source in traditional Chinese medicine(TCM),and by integrating the theory of kidney dominating bone,liver dominating tendon,and meridian sinew of TCM as well as the bone resorption and collapse theory,and non-uniform settlement theory and lower-limb musculoskeletal bowstring structure theory of modern orthopedics,the pathogenesis of osteonecrosis of the femoral head(ONFH)under the system of non-uniform settlement during bone resorption and multidimensional composite bowstring working in coordination with the theory of liver-kidney and muscle-bone was explored.The key to the TCM pathogenesis of ONFH lies in the deficiency of the liver and kidney,and then the imbalance of kidney yin-yang leads to the disruption of the dynamic balance of bone formation and bone resorption mediated by osteoblasts-osteoclasts,which manifests as the elevated level of bone metabolism and the enhancement of focal bone resorption in the femoral head,and then leads to the necrosis and collapse of the femoral head.It is considered that the kidney dominates bone,liver dominates tendon,and the tendon and bone together constitute the muscle-bone-joint dynamic and static system of the hip joint.The appearance of collapse destroys the originally balanced muscle-bone-joint system.Moreover,the failure of liver blood in the nourishment of muscles and tendons further exacerbates the imbalance of the soft tissues around the hip joint,accelerates the collapse of the muscle-bone-joint dynamic and static system,speeds up the process of femoral head collapse,and ultimately results in irreversible outcomes.Based on the above pathogenesis,the systematic integrative treatment of ONFH should be based on the TCM holistic concept,focuses on the focal improvement of internal and external blood circulation of the femoral head by various approaches,so as to rebuild the coordination of joint function.Moreover,attention should be paid to the physical constitution of the patients,and therapy of tonifying the kidney and regulating the liver can be used to restore the balance between osteogenesis and osteoblastogenesis,and to reconstruct the muscle-bone-joint system,so as to effectively delay or even prevent the occurrence of ONFH.
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BACKGROUND:Periodontitis is an inflammatory and destructive disease with plaque biofilm as the main pathogenic material,which occurs in the gingiva,periodontal ligament,alveolar bone and cementum.The antigen of bacterial complex and its secreted toxin and enzyme directly lead to the destruction of periodontal tissue and trigger the host's immune response,causing indirect damage to the body tissue.Silence information regulatory factors(Sirtuins,SIRTs)play an important role in anti-aging,anti-oxidative stress,regulating inflammation,and mediating autophagy,and are closely related to the occurrence and development of periodontitis. OBJECTIVE:To review the research status of Sirtuins in periodontitis. METHODS:The first author used the computer to search the relevant research regarding the role of Sirtuins in periodontitis in PubMed,Web of Scene,CNKI and WanFang databases.The key words were"Sirtuins,Sirtuin1-7,periodontitis"in English and Chinese.After literature screening,57 articles were included for review and analysis. RESULTS AND CONCLUSION:SIRT1,SIRT2,SIRT3,and SIRT6 participate in regulating the occurrence and development of periodontitis.Inhibition of SIRT1 expression may be the target of periodontitis treatment,while overexpression of SIRT1 can inhibit periodontitis and protect periodontal tissue.The activator of SIRT1 can reduce the inflammation of periodontal tissue and improve the systemic pathological changes caused by periodontitis.SIRT2 is involved in nicotinamide phosphoribosyltransferase-mediated periodontal inflammation and plays a role in the treatment and prognosis of periodontal diseases.SIRT3 can improve age-related periodontal disease.Gastrodin promotes the osteogenic differentiation of periodontal ligament stem cells through the up-regulation of SIRT3.The activator of SIRT3 reduces the damage of periodontitis to periodontal and renal tissues by regulating the level of autophagy in the cells.SIRT6 can inhibit the inflammatory reaction of periodontal tissue and inhibit the differentiation and mineralization of cementoblasts.SIRT6 is beneficial to the prognosis of periapical periodontitis.The relationship between SIRT4,SIRT5,SIRT7 and periodontitis is rarely reported.
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BACKGROUND:Abnormal activation of osteoclasts plays an important role in the bone destruction due to spinal tuberculosis.During the pathogenesis of osteoporosis,miR-155 knockdown activates adenosine phosphate-dependent protein kinase(AMPK)by increasing the expression of leptin receptors,thereby inhibiting osteoclast differentiation and bone resorption.However,the role of miR-155/leptin receptor(LEPR)/AMPK axis in the bone destruction due to spinal tuberculosis remains unclear. OBJECTIVE:To investigate the role and mechanism of miR-155/LEPR/AMPK axis in tuberculin-induced osteoclast formation. METHODS:RAW264.7 cells were cultured and treated with different concentrations of purified protein derivative(PPD)(1.0,2.5,5.0,10.0 IU/mL)and transfected with negative control(NC)sequence or miR-155 inhibitor,NC siRNA sequence or LEPR siRNA sequence.Tartrate resistant acid phosphatase staining was used to detect the number of osteoclasts.Fluorescence quantitative PCR was used to detect the expression of miR-155.Western blot was used to detect the expression of LEPR and p-AMPK.Double luciferase reporter gene was used to verify miR-155 targeting LEPR. RESULTS AND CONCLUSION:Compared with the control group,the number of osteoclasts and the expression level of miR-155 significantly increased,while the expression level of LEPR and p-AMPK significantly decreased in 2.5,5.0,and 10.0 IU/mL PPD groups(P＜0.05).Compared with NC+5.0 IU/mL PPD group,the number of osteoclasts and the expression level of miR-155 significantly decreased,while the expression level of LEPR and p-AMPK significantly increased in the miR-155 inhibitor+5.0 IU/mL PPD group(P＜0.05).Compared with the NC group,the fluorescence activity of LEPR wild-type double luciferase reporter gene was increased in the miR-155 inhibitor group,and decreased in the miR-155 mimic group(P＜0.05).Compared with si-NC+miR-155 inhibitor+5.0 IU/mL PPD group,the expression level of miR-155 had no significant change,the number of osteoclasts significantly increased,and the expression levels of LEPR and p-AMPL significantly decreased in si-LEPR+miR-155 inhibitor+5.0 IU/mL PPD group(P＜0.05).To conclude,tuberculin can induce osteoclast formation by increasing miR-155 expression and inhibiting downstream LEPR expression and AMPK activation.
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BACKGROUND:Tumor necrosis factor-α is a broadly acting inflammatory cytokine that plays an important role in the immune inflammatory response of the body.The current study concluded that tumor necrosis factor-α has significant biological effects on a variety of bone tissue cells. OBJECTIVE:To summarize the expression and action pathways of tumor necrosis factor-α in osteoblastic and osteoclastic cells to further elucidate the regulatory role of tumor necrosis factor-α on bone tissue cells. METHODS:PubMed and CNKI were searched until March 2023,and the Chinese search terms included"tumor necrosis factor α,osteoblast,osteoclast,osteoclast,osteoprogenitor";the English search terms included"TNF-α,osteoblast,osteoclast,osteocyte,osteoprogenitor cell".The corresponding criteria were established according to the research needs,and the final literature was screened.Finally,77 articles were included for review. RESULTS AND CONCLUSION:(1)Tumor necrosis factor-α is participating in regulating the recruitment,appreciation,and differentiation of osteoprogenitor cells,but leads to osteoprogenitor cell stripping and death under specific environments.It also participates in bone resorption directly or indirectly through secreted enzymes.(2)Tumor necrosis factor-α can increase the level of inflammatory factors in the environment by activating relevant signaling pathways in osteoclast lineage cells or directly induce the generation of osteoclasts in specific environments.(3)Tumor necrosis factor-α can inhibit osteogenic differentiation by activating nuclear factor-κB signaling pathway,inhibiting the expression of transcription factors such as RUNX2 and Osterix,and inducing apoptosis and necrotizing apoptosis in osteoblasts.(4)Tumor necrosis factor-α inhibits osteogenesis and promotes osteoclastogenesis by activating the nuclear factor-κB signaling pathway in osteocytes and inducing cytokines such as RANKL,SOST,and DKK1,while enhancing apoptosis of the osteocytes,as well as bone resorption around the apoptotic bone tissue.(5)Taken together,the effect of tumor necrosis factor-α in bone tissue is mainly to inhibit osteogenesis and promote osteoclastosis.The biological effect of tumor necrosis factor-α in bone tissue cells is usually dependent on the activation of tumor necrosis factor receptor and nuclear factor-κB signaling pathways.(6)The interaction of tumor necrosis factor-α with other tissue cell types surrounding bone tissue and its role in bone immune regulation still deserve attention in future studies.
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BACKGROUND:Osteoprotegerin(OPG)/receptor activator of nuclear factor-κB(RANK)/receptor activator of nuclear factor-κB ligand(RANKL)are important cytokines for coupling osteoclast and osteoblast differentiation and activation,and are key factors for regulating bone metabolism,which affect the immune system,bone regeneration and remodeling,and are closely related to the physiological and pathological remodeling of the alveolar bone. OBJECTIVE:To analyze the effects of the OPG/RANK/RANKL signaling pathway on alveolar bone remodeling and the progress in its targeted therapy application in the dental field. METHODS:We searched relevant articles included in CNKI and PubMed databases with the keywords of"OPG,anti-RANKL antibody,RANKL,periodontitis,orthodontic tooth movement,implant,tooth eruption,periapical lesion,alveolar bone resorption"in Chinese and English,respectively.A total of 63 articles were finally included for review. RESULTS AND CONCLUSION:Anti-RANKL therapy can treat oral diseases by targeting the inhibition of osteoclast formation and alveolar bone absorption.Local and systemic anti-RANKL therapy can inhibit the progression of periodontitis,peri-implantitis and periapical lesions,and it also plays an important role in preventing orthodontic relapse,strengthening orthodontic anchorage and implant osseointegration.RANKL therapy can treat oral diseases by promoting osteoclast differentiation and alveolar bone absorption.RANKL treatment can accelerate orthodontic tooth movement,shorten the treatment cycle and reduce the incidence of orthodontic complications.Although there are limitations in anti-RANKL therapy,they can be avoided by rational applications,such as excluding local and systemic risk factors before treatment,regular oral maintenance and avoiding traumatic alveolar surgery as much as possible during treatment.
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BACKGROUND:Exosomes are vesicle-like structures secreted by cells into extracellular compartments in the form of cytosol,which contain a large amount of microRNAs with important intercellular communication roles.MicroRNAs in exosomes rely on exosome transport and are able to enter target cells to exert important biological regulatory effects.In common bone and joint diseases,abnormal or damaged bone metabolism releases a large number of exosomes,while some exosome-derived microRNAs also promote the progression of osteoarthritis.Therefore,exosome-derived microRNAs are closely related to the skeletal system and are important for the development as well as diagnosis and treatment of many osteoarticular diseases. OBJECTIVE:To review the research progress of exosome-derived microRNAs in bone metabolism and bone and joint diseases. METHODS:Using"exosomes,extracellular vesicle,microRNA,miRNA,bone,bone diseases,bone formation,bone regeneration,bone resorption,bone destruction"as Chinese and English search terms,articles were searched on CNKI,Metasys,and PubMed databases.Finally,86 articles were included for summarization. RESULTS AND CONCLUSION:Exosome-derived microRNAs can regulate bone metabolism by affecting bone formation and bone resorption,and are closely related to the development of bone and joint diseases such as fracture healing,osteoporosis,osteoarthritis,rheumatoid arthritis,osteonecrosis of the femoral head,and osteosarcoma.Exosome-derived microRNAs will be an effective means of diagnosis and treatment of certain bone and joint diseases in the future.However,the current research on exosome-derived microRNAs in osteoarthritic diseases is limited,and more explorations and researches are still needed to diagnose and treat osteoarthritic diseases using exosome-derived microRNAs.
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BACKGROUND:The application of orthodontic force triggers autophagy in the periodontal tissue via diverse signaling pathways,augmenting or attenuating the activity of relevant cell types such as periodontal ligament cells,osteocytes,osteoclasts,and osteoblasts,thus facilitating the process of periodontal remodeling. OBJECTIVE:To review the research progress in orthodontic force mediated autophagy in periodontal tissue and its impact on orthodontic tooth movement. METHODS:The PubMed,Web of Science,China Biology Medicine disc and CNKI were searched for literature published from 2010 to 2023 to summarize the progress in orthodontics-related autophagy.And 76 papers were finally included in the analysis and discussion. RESULTS AND CONCLUSION:Orthodontic force can trigger a series of biochemical signal changes through periodontal mechanical receptors and aseptic inflammation they cause,leading to autophagy in periodontal tissue.Subsequently,autophagy generates corresponding feedback through cascaded amplified signaling pathways such as Phosphoinositide 3-kinase/protein kinase B,Hippo,and mitogen-activated protein kinase pathways,promoting periodontal tissue remodeling and ultimately achieving tooth movement and stability.Orthodontic force-induced autophagy can differentially regulate bone resorption on the tooth pressure side and bone formation on the tension side.Related targets have good prospects in the clinical application of orthodontic treatment.Orthodontics and autophagy have complex mechanisms.However,existing research has only focused on exploring the role of autophagy in orthodontic tooth movement.Further exploration is needed to investigate the mutual regulatory effects between autophagy and orthodontic tooth movement,as well as the interactions between upstream mechanical receptors and signaling pathways involved in related pathways.
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@#Magnetic fields are safe and used in noninvasive physical therapies. Numerous studies have confirmed that magnetic fields have good osteogenic effects and certain value for clinical application in accelerating orthodontic tooth movement, promoting bone-implant integration, promoting fracture healing and improving the effects of distraction osteogenesis. Magnetic fields are expected to become applied as effective auxiliary methods for treating oral diseases. To support the clinical application of magnetic fields, this article reviews the applications of magnetic fields in the oral cavity, the biological effects on bone cells and the molecular mechanisms through which magnetic fields regulate bone metabolism. The biological effects of magnetic fields on bone cells include promoting osteogenesis by osteoblasts and mesenchymal stem cells and inhibiting bone resorption by osteoclasts. At the molecular level, bone cells sense and respond to magnetic stimulation, and through various mechanisms, such as displacement currents, Lorentz forces, and free radical pair effects, stimuli are transformed into biologically recognizable electrical signals that activate complex downstream signaling pathways, such as the P2 purinergic receptor signaling pathway, adenosine receptor signaling pathway, transforming growth factor-β receptor signaling pathway, mammalian target of rapamycin (mTOR) pathway, and Notch pathway. In addition, magnetic parameters, which are the factors affecting the osteogenic effects of magnetic fields, are discussed. However, the mechanisms of the osteogenic effects of magnetic fields are unclear, and further studies of these mechanisms could provide effective strategies for bone regeneration and periodontal tissue regeneration. In addition, considering the target of magnetic field therapies, combination with other drugs could lead to new strategies for the treatment of oral diseases.
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ABSTRACT One of the most common dental procedures is tooth extraction; however, the bone defect resulting from the process is only partially restored, leading to considerable bone loss. To rehabilitate a fully or partially edentulous patient, we must handle these sites with delicate surgical procedures. There is a large literature presenting attempts to overcome the negative effects of a dental extraction, with the aim of reducing tissue volume loss or restoring the alveolar architecture. In this context, Partial Extraction Therapy (PET) represents a subgroup of interventions to prevent bone loss after extraction using the tooth itself to prevent alveolar bone loss. This literature review aims to make a survey of the published articles on PET, with an emphasis on socket shield technique, and to explain the other techniques such as root burial, pontic-shield and proximal socket-shield, their indications and counter indications in order to deepen the knowledge of these techniques. To identify the included or considered studies, we adopted a detailed search strategy for MEDLINE and Cochrane Library focused in the last 31 years, whose language was English, Spanish or Portuguese. This text presents an analysis of current data regarding the alternatives for alveolar preservation and the installation of immediate implants in these areas, presenting the possibility of a different surgical technique. However, due to the immaturity and lack of conclusive scientific evidence regarding the predictability of the procedures, it is considered that the use of the socket shield technique must be done in an extremely cautious way.
RESUMO Um dos procedimentos odontológicos mais comuns é a extração dentária, contudo, , o defeito ósseo decorrente do processo é apenas parcialmente restaurado, levando a uma perda ossea volumétrica consideravel. Para reabilitar um paciente totalmente ou parcialmente desdentado, devemos manusear estes sitios com intervenções cirúrgicas delicadas. Há uma vasta literatura apresentando tentativas de transpor os efeitos negativos de uma extração dentária, com o objetivo de diminuir a perda volumétrica tecidual ou restaurar a arquitetura alveolar. Neste contexto, a Terapia de Extração Parcial (TEP) representa um subgrupo de intervenções para prevenir a perda óssea após exodontia, usando o próprio dente para prevenir a perda óssea alveolar. Essa revisão de literatura tem por objetivo fazer um levantamento dos artigos publicados sobre as TEP, com ênfase na técnica de socket shield, e explanar a cerca das demais técnicas como sepultamento radicular, pontic-shield e proximal socket-shield, suas indicações e contra-indicações, a fim de aprofundar o conhecimento dessas técnicas. Para a identificação dos estudos inclui?dos ou considerados, adotamos a estrate?gia de busca detalhada para os bancos MEDLINE e Biblioteca Cochrane nos u?ltimos 31 anos, cujo idioma fosse o ingle?s, espanhol ou o portugue?s. Este texto, apresenta uma análise de dados atuais a respeito das alternativas para a preservação alveolar e instalação de implantes imediatos nestas áreas, apresentando a possibilidade de uma técnica cirúrgica diferenciada. No entanto, devido a imaturidade e falta de comprovação cientifica contundente a respeito da previsibilidade dos procedimentos, considera-se que o emprego da técnica de socket shield deve ser feito de forma cautelosa.
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La enfermedad periodontal es una de las principales causas de pérdida dentaria. Clínicamente, esta patología, mediada por la desregulación del sistema inmune producto de una disbiosis ocurrida en el surco gingival, inicia con la inflamación de la encía y evoluciona con el daño irreversible de los tejidos que rodean el diente. El hueso alveolar es uno de los tejidos afectados esta patología, esto debido a la activación de osteoclastos por la sobreexpresión de la proteína RANKL en el huésped. El propósito de este trabajo es determinar el nivel de sobreexpresión de RANKL, en un modelo de células tumorales U2OS, frente a la infección con Porphyromonas gingivalis y Prevotella intermedia. Para identificar el nivel de RANKL, se definieron cuatro grupos: Un grupo control, no tratado; Grupo PG, tratado con P. gingivalis; Grupo PI, tratado con P. Intermedia; y un grupo PG+PI, tratado con ambas bacterias. El nivel relativo de la proteína RANKL fue determinado en el sobrenadante y en los extractos celulares de manera independiente, mediante la técnica Western blot. En sobrenadantes, el grupo PG mostró mayores niveles de RANKL comparados con PI (p < 0,05). En extractos celulares los niveles fueron mayores en el grupo PG+PI (p < 0,05). El grupo PI mostró los niveles más bajos de RANKL. La infección polimicrobiana resulta en una mayor expresión de RANKL en células tumorales U2OS, mientras que frente a la infección P. gingivalis, se observó mayor cantidad de RANKL soluble.
SUMMARY: Periodontal disease is one of the main causes of tooth loss. Clinically, this pathology, mediated by the deregulation of the immune system due to a dysbiosis occurred in the gingival sulcus, begins with the inflammation of the gum and evolves with the irreversible damage of the tissues that surround the tooth. Alveolar bone is one of the most affected tissues by this disease, due to the activation of osteoclasts by the upregulation of RANKL in the host. The aim of this study is to determine the increase of RANKL, in a U2OS tumor cells model, inoculated with Porphyromonas gingivalis and Prevotella intermedia. To identify the level of RANKL, four groups were defined: A control group, not treated; PG group, treated with P.gingivalis; PI group, treated with P. intermedia; and a PG+PI group, treated with both bacteria. The relative level of RANKL was determined in the supernatant and cell extracts independently, using the Western blot technique. In supernatants, the PG group showed higher RANKL levels compared to PI (p < 0.05). In cell extracts the levels were higher in the PG+PI group (p < 0.05.). The PI group showed the lowest levels of RANKL.Polymicrobial infection results in a greater expression of of soluble RANKL was observed.
Subject(s)
Periodontal Diseases/microbiology , Bacteria, Anaerobic/physiology , Bone Resorption/microbiology , RANK Ligand/metabolism , Cells, Cultured , Blotting, Western , Porphyromonas gingivalis/physiology , Prevotella intermedia/physiology , Cell Line, Tumor , Electrophoresis , RANK Ligand/analysisABSTRACT
OBJECTIVES@#This study aimed to evaluate the long-term clinical efficacy of simple taper retentive implants in the posterior dental area after immediate implantation for 5-7 years.@*METHODS@#Selected from January 2015 to December 2017 in the Fourth Affiliated Hospital of Nanchang University dental clinic line tooth area immediately after the implant prosthesis, a total of 38 patients, 53 implants, were deep into (bone under 2 mm or higher) and the upper structure was repaired. In addition, after the completion of tracking observation of 60-90 months, the implant surrounding bone health was recorded and analyzed.@*RESULTS@#After 5-7 years of follow-up, 1 of the 53 implants failed to fall out, and the implant retention rate was 98.1%. The amount of bone resorption in the proximal and distal margins 5-7 years after implant restoration was (0.16±0.94) mm and (-0.01±1.29) mm, respectively, and the difference in bone height between the proximal and distal margins of the implant and the immediate post-restoration period was not statistically significant (P>0.05). No statistically significant differences were found in the effects of periodontitis, implant site inflammation, and smoking on peri-implant marginal bone resorption (P>0.05).@*CONCLUSIONS@#The single taper-retained implant broadens the indications for immediate implant placement in the posterior region, and its deep sub-osseous placement (≥2 mm below the bone) avoids to a certain extent the disturbance of the implant by external stimuli and the exposure of the cervical abutment of the implant, with the good long-term stability of the marginal bone around the implant.
Subject(s)
Humans , Dental Implantation, Endosseous , Dental Implants , Immediate Dental Implant Loading , Follow-Up Studies , Dental Implants, Single-Tooth , Alveolar Bone Loss/surgery , Treatment Outcome , Dental Prosthesis, Implant-Supported , Dental Restoration FailureABSTRACT
Objective:To explore the association of bone resorption marker β carboxyterminal peptide of collagen Ⅰ (β-CTX) with hypercalcemia in patients with Graves′ disease (GD).Methods:287 patients with GD who were hospitalized in the endocrinology department of Fuyang People′s Hospital from January 2021 to December 2021 were divided into control group ( n=251) and hypercalcemia group ( n=36) according to the corrected blood calcium level. The clinical data and serum β-CTX level of the two groups were compared. Logistic regression model was used to analyze the risk factors of hypercalcemia in GD patients. Pearson correlation was used to analyze the correlation between serum β-CTX level and other indexes. Results:Of the 287 GD patients, 36 were diagnosed as hypercalcemia, and the incidence of hypercalcemia was 12.54%. The levels of free triiodothyronine (FT3), free thyroxine (FT4), blood phosphorus (P) and β-CTX in hypercalcemia group were higher than those in control group, and the total parathyroid hormone (iPTH) in hypercalcemia group were lower than those in control group (all P<0.05). Multivariate Logistic regression analysis showed that FT3 ( OR=1.283, 95% CI: 1.049-1.570, P<0.05), iPTH ( OR=0.924, 95% CI: 0.863-0.989, P<0.05), β-CTX ( OR=2.488, 95% CI: 1.193-5.189, P<0.05) were the influencing factors for hypercalcemia in GD patients. Pearson correlation analysis showed that β-CTX was positively correlated with FT3, FT4, blood calcium, P, alkaline phosphatase (ALP), total procollagen type I amino end terminal peptide (PINP), N-bone-gamma-carboxyglutamic-acid-containing proteins (N-MID) and 25(OH)D, and negatively correlated with iPTH (all P<0.05). Conclusions:β-CTX is highly expressed in the serum of GD patients with hypercalcemia, which is a risk factor for the occurrence of hypercalcemia in GD patients.
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Osteoporotic fractures secondary to osteoporosis increase very rapidly in incidence, and have become a major cause of disability and mortality in the elderly population. Currently, there have no standard guidelines for perioperative management, surgery and postoperative rehabilitation, causing multiple complications and poor therapeutic outcome. The authors previously proposed bone repair strategies including active anti-osteoporosis, adequate bone grafting and bone healing acceleration, namely "three-in-one" bone repair strategy. The care steps in osteoporotic fracture surgery inluded perioperative management, operative precaution, and postoperative prevention of secondary fractures. With this in mind, the authors further discussed the detailed application of "three-in-one" bone repair strategy including perioperative active anti-osteoporosis treatment, early rehabilitation training, standardized internal fixation selection, standard bone grafting methods and prevention of secondary complications, so as to promote the standardized treatment of osteoporotic fractures and improve the prognosis.
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Objective:To explore the changes of bone turnover markers induced by sleep deprivation (SD) and the effect of melatonin supplementation on the bone turnover status.Methods:Six-week-old Wistar male rats were divided into SD, normal control (NC), and melatonin supplementation (SD+ MT) groups. Acute SD model was established using a modified multi-level bench method. The bone turnover markers, corticosterone, and melatonin in serum as well as Cathepsin K(CTSK) mRNA expression in bone tissue were tested.Results:Acute SD disrupted the balance between bone formation and bone absorption evidenced by rapid decreased serum procollagen type Ⅰ N-terminal propeptide (PⅠNP) levels and increased β cross-linked C-telopeptide of type Ⅰ collagen (β-CTX) levels ( P=0.003) from 24 h to 72 h. The exogenous melatonin treatment decreased β-CTX [(512.4±95.8) ng/mL vs (696.0±76.5) ng/mL, P=0.004] and the osteoclast-related gene CTSK mRNA level after 72 h SD. Conclusions:Acute SD accelerates bone resorption, which could be partially alleviated by melatonin supplementation.
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Osteosclerosis is a rare hereditary bone metabolic disease, characterized by increased bone mass and density caused by bone resorption disorders, and any abnormal mutation involving osteoclast maturation or function will lead to the occurrence of osteopetrosis. Clinically, the prevalence of autosomal dominant osteopetrosis type Ⅱ(ADO-Ⅱ) is higher than that of other types of osteopetrosis, which involves multiple systems such as endocrine, bone, blood, nerve, ear-nose-throat, and oral cavity. Disease progression is insidious and easily overlooked, and there is no standard treatment. This article summarizes the clinical characteristics, examination data, diagnosis and treatment process of the two patients, analyzes multi-system symptoms, pathogenesis and treatment principles of the disease to improve the management of patients with ADO-Ⅱ.
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@#It has been traditionally believed that a 1:1 cortical bone remodeling/tooth movement ratio has been preserved during orthodontic treatment for tooth movement, with the alveolar bone on the tension side growing and the alveolar bone on the pressure side resorbing to maintain the balance of the alveolar bone. However, recent studies have shown that alveolar bone loss has been found in patients who have undergone orthodontic treatment, suggesting that the alveolar bone does not change as the teeth change over time. Whether the morphology of the alveolar bone will change when the anterior teeth are moved has been the clinical focus. The changes of anterior alveolar bone in patients who have undergone tooth extraction after orthodontic treatment were summerized by literature review in this paper. The results of the review showed that the alveolar bone at the lingual/palatal root-cervical site of the anterior root is more prone to bone loss after extensive movement of the anterior teeth. With the development of imaging technology, CBCT is now more commonly used for analysis instead of two-dimensional images for measurement, as its results are more accurate. However, there are few multifactorial studies in which CBCT has been used to assess the morphological changes in the alveolar bone. The focus of future research is to compare the long-term changes in the anterior alveolar bone of patients of different ages based on three-dimensional imaging, and to study the correlation between different skeletal features, tooth movement patterns and alveolar bone remodeling.
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@#Osteoclasts are the only cells responsible for bone resorption in the body, and osteoblasts are the main cells responsible for bone regeneration in the body. Under physiological conditions, these cells maintain a dynamic balance to maintain bone homeostasis. It was widely believed that the imbalance of bone metabolism is mainly affected by the expression of related inflammatory factors. However, with the gradual expansion of related studies in recent years, autophagy has been shown to be closely related to the differentiation, apoptosis and functions of osteoclasts and osteoblasts. AMP-activated protein kinase (AMPK) is an important regulator of energy metabolism in vivo and is involved in the regulation of autophagy and bone homeostasis in bone metabolism-related cells. Periodontitis is a chronic infectious disease, and its typical symptoms are alveolar bone resorption. At present, controlling the level of periodontal inflammation and alveolar bone resorption more effectively in clinical practice remains a challenge. The detection of AMPK and autophagy levels in bone metabolism-related cells shows certain prospects for the clinical prevention and treatment of periodontitis in the future. Therefore, this article reviews the regulation of periodontal inflammation levels and bone homeostasis through cell autophagy related to AMPK-mediated bone metabolism.
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In this study, the ovarian surgery (ovariectomy, OVX) was used to establish the osteoporosis mice model of primary menstruation, in order to evaluate the protective effects and mechanisms of Zhibai Dihuang decotion on postmenopausal osteoporosis (PMOP). The animal experimental protocol has been reviewed and approved by Laboratory Animal Ethics Committee of Jinan University (number: 20210315-03), in compliance with the Institutional Animal Care Guidelines. C57BL/6 mice were divided into five groups, including Sham group, OVX group, low (32 g·kg-1·day-1) and high dose (64 g·kg-1·day-1) of Zhibai Dihuang decotion groups, positive drug group (alendronate, 9.9 mg·kg-1·q3d). After modeling, mice were given medication intervention for 8 weeks, and then femoral and tibial tissues were taken to detect indicators such as bone microstructure, bone resorption, and oxidative stress. The experimental results showed that after Zhibai Dihuang decotion administration, the bone microstructure damage caused by OVX surgery was alleviated, and the relevant parameters bone mineral density (BMD), bone volume/total volume (BV/TV), trabecular number (Tb. N) and connectivity density (Conn. D) both significantly increased. At the same time, the number of TRAP positive osteoclasts decreased significantly, and the levels of proteins and genes related to osteoclast differentiation decreased, indicating that Zhibai Dihuang decoction could inhibit the increased activity of osteoclast caused by OVX. Afterwards, network pharmacology was used to construct the active compound action target network of Zhibai Dihuang decotion, and it was found that the target genes of its active ingredients were closely related to the oxidative stress pathway. Finally, the detection results of oxidative stress levels in bone tissues showed that after treatment with Zhibai Dihuang decotion, the levels of oxidative stress products 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA) in bone tissues of mice significantly decreased, while the levels of antioxidant stress substance L-glutathione (GSH) increased. These above results indicated that Zhibai Dihuang decotion can regulate the level of oxidative stress in the body and inhibit osteoclast activity, which played a therapeutic role in PMOP, as well as provided theoretical basis for the prevention and treatment of PMOP with traditional Chinese medicine.
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The ubiquitin-proteasome system (UPS) dedicates to degrade intracellular proteins to modulate demic homeostasis and functions of organisms. These enzymatic cascades mark and modifies target proteins diversly through covalently binding ubiquitin molecules. In the UPS, E3 ubiquitin ligases are the crucial constituents by the advantage of recognizing and presenting proteins to proteasomes for proteolysis. As the major regulators of protein homeostasis, E3 ligases are indispensable to proper cell manners in diverse systems, and they are well described in physiological bone growth and bone metabolism. Pathologically, classic bone-related diseases such as metabolic bone diseases, arthritis, bone neoplasms and bone metastasis of the tumor, etc., were also depicted in a UPS-dependent manner. Therefore, skeletal system is versatilely regulated by UPS and it is worthy to summarize the underlying mechanism. Furthermore, based on the current status of treatment, normal or pathological osteogenesis and tumorigenesis elaborated in this review highlight the clinical significance of UPS research. As a strategy possibly remedies the limitations of UPS treatment, emerging PROTAC was described comprehensively to illustrate its potential in clinical application. Altogether, the purpose of this review aims to provide more evidence for exploiting novel therapeutic strategies based on UPS for bone associated diseases.
ABSTRACT
A infecção endodôntica ocorre a após contaminação do tecido pulpar levando à uma colonização bacteriana dos canais radiculares resultando em uma resposta inflamatória dos tecidos periapicais e formação de uma lesão periapical, a periodontite apical (PA). O tabagismo, por sua vez, tem impactos prejudiciais à saúde oral e sistêmica sendo considerado um importante fator de risco para as doenças periodontais. Este trabalho tem por finalidade investigar a influência do tabagismo no desenvolvimento da periodontite apical em ratos. Trinta e dois ratos machos Wistar foram divididos em 4 grupos experimentais (n=8): Controle (sem periodontite apical induzida e sem inalação da fumaça do cigarro); FU (com inalação a fumaça do cigarro); PA (com periodontite apical induzida); FU+PA (com inalação a fumaça do cigarro e periodontite apical induzida). Para a inalar a fumaça do cigarro, grupo de cinco animais permaneceram em uma câmara de tabagismo inalando a fumaça de 10 cigarros por 8 minutos, três vezes ao dia, durante 50 dias. Decorridos 20 dias de inalação de fumaça do cigarro, foi realizada a cirurgia para indução da periodontite apical nos animais do grupo PA e FU+PA, no primeiro molar inferior direto, o qual permaneceu aberto na cavidade bucal por 30 dias. Nesses 30 dias subsequentes da indução da PA, os animais do grupo FU+PA e FU continuaram com a inalação a fumaça do cigarro. No 50º dia, os animais foram eutanasiados e coletados amostras de tecido hematológico para avalição dos níveis séricos de nicotina, cotinina, fosfatase alcalina, cálcio, fósforo, série vermelha e série branca. As hemimandibula removidas foram escaneadas em microtomógrafo para avaliar o volume da destruição óssea e processadas histologicamente para avaliação do perfil inflamatório e expressão das citocinas IL-6, IL-1ß, TNF-α e dos marcadores do metabolismo ósseo RANKL e OPG. Os dados foram tabulados e aplicados os testes estatísticos de Mann-Whitney para os dados não paramétricos e teste t para os dados paramétricos, a um nível de significância de P< 0.05. Com relação a análise histológica o grupo FU+PA apresentou infiltrado inflamatório mais intenso em relação aos demais grupos (P< 0,05). As citocinas pró-inflamatórias IL-6, IL-1ß, TNF-α apresentaram alto padrão de imunomarcação para o grupo FU+PA (P< 0,05). A análise histométrica mostrou maior área de reabsorção óssea no grupo FU+PA, assim como na análise microtomográfica (P< 0,05). As citocinas RANKL esteve mais expressa no grupo FU+PA (P< 0,05) e OPG teve maior expressão no grupo PA (P< 0,05). Na análise hematológica houve um aumento na concentração de hemácias, hemoglobina e leucócitos para o FU+PA (P< 0,05). Os níveis séricos de cálcio foram menores no FU+PA (P> 0,05), a fosfatase alcalina e o cálcio se manteve constante em todos os grupos experimentais (P> 0,05). A concentração sérica de nicotina e cotinina no grupo FU e FU+PA foram compatíveis com fumante humano(AU)
Endodontic infection occurs mainly after pulp tissue contamination by a carious process, leading to bacterial colonization of root canal system and inflammatory response of periapical tissues, followed by formation of apical periodontitis (AP). It is widely known that smoking has harmful impacts on oral and systemic health and is considered a risk factor for periodontal diseases. The objective of this research was to investigate the influence of smoking on the development of AP in rats. Thirty-two male Wistar rats were divided into 4 experimental groups (n = 8): C - Control (no induced AP and no cigarette smoke inhalation); CSI (cigarette smoke inhalation); AP (induced apical periodontitis); CSI + AP (cigarette smoke inhalation and induced apical periodontitis). To inhale cigarette smoke, group with five animals remained in a smoking chamber inhaling smoke from 10 cigarettes for 8 minutes, three times daily, for 50 days. After 20 days of cigarette smoke inhalation, pulp chamber access was performed to induce apical periodontitis in the first mandibular right molar, which remained with pulp chamber exposed to oral cavity for 30 days in animals in the AP and CSI + AP group. During these 30 days after the AP induction, animals in the CSI + AP and CSI group continued to inhale cigarette smoke. On the 50th day, animals were euthanized and blood sample collected to assess serum levels of nicotine, cotinine, alkaline phosphatase, calcium, phosphorus, red series and white series. The hemimandibles were removed and scanned in microtomograph to assess bone volume and histologically processed to assess inflammatory profile and expression of cytokines IL-6, IL-1ß, TNF-α and bone metabolism markers RANKL and OPG. Data were tabulated and statistically analyzed using Mann-Whitney tests for nonparametric data and analysis of variation test for parametric data, with a significance level of P< 0.05. Regarding histological analysis, CSI+AP group showed more intense inflammatory infiltrate compared to other groups (P < 0.05). Histometric analysis showed a larger area of bone resorption in the CSI + AP group, also observed in the microtomographic analysis (P< 0.05). Group CSI+AP had elevated pro-inflammatory cytokines IL-6, IL-1ß, TNF-α expression (P< 0.05). The RANKL cytokines were also more expressed in the CSI+AP group (P< 0.05), while OPG was more expressed in the AP group (P< 0.05). The hematological analysis revealed an increase in the concentration of red blood cells, hemoglobin, and leukocytes for CSI+AP (P< 0.05). Serum calcium levels were lower in CSI+AP (P> 0.05), and alkaline phosphatase and calcium remained constant in all experimental groups (P> 0.05). The serum concentrations of nicotine and cotinine in the CSI and CSI+AP group were compatible with human smokers(AU)