Recent advances of exosomal circRNAs in cancer and their potential clinical applications.

Circular RNA (circRNA) is a type of non-coding RNA that forms a covalently closed, uninterrupted loop. The expression of circRNA differs among cell types and tissues, and various circRNAs are aberrantly expressed in a variety of diseases, including cancer. Aberrantly expressed circRNAs contribute to disease progression by acting as microRNA sponges, functional protein sponges, or novel templates for protein translation. Recent studies have shown that circRNAs are enriched in exosomes. Exosomes are spherical bilayer vesicles released by cells into extracellular spaces that mediate intercellular communication by delivering cargoes. These cargoes include metabolites, proteins, lipids, and RNA molecules. Exosome-mediated cell-cell or cell-microenvironment communications influence the progression of carcinogenesis by regulating cell proliferation, angiogenesis, metastasis as well as immune escape. In this review, we summarize the current knowledge about exosomal circRNAs in cancers and discuss their specific functions in tumorigenesis. Additionally, we discuss the potential value of exosomal circRNAs as diagnostic biomarkers and the potential applications of exosomal circRNA-based cancer therapy.

Targeted regulation of FoxO1 in chondrocytes prevents age-related osteoarthritis via autophagy mechanism.

Autophagy is designated as a biological recycling process to maintain cellular homeostasis by the sequestration of damaged proteins and organelles in plasma and cargo delivery to lysosomes for degradation and reclamation. This organelle recycling process promotes chondrocyte homeostasis and has been previously implicated in osteoarthritis (OA). Autophagy is widely involved in regulating chondrocyte degeneration markers such as MMPs, ADAMSTs and Col10 in chondrocytes. The critical autophagy-related (ATG) proteins have now been considered the protective factor against late-onset OA. The current research field proposes that the autophagic pathway is closely related to chondrocyte activity. However, the mechanism is complex yet needs precise elaboration. This review concluded that FoxO1, a forkhead O family protein, which is a decisive mediator of autophagy, facilitates the pathological process of osteoarthritis. Diverse mechanisms regulate the activity of FoxO1 and promote the initiation of autophagy, including the prominent AMPK and Sirt-2 cellular pathways. FoxO1 transactive is regulated by phosphorylation and acetylation processes, which modulates the downstream ATGs expression. Furthermore, FoxO1 induces autophagy by directly interacting with ATGs proteins, which control the formation of autophagosomes and lysosomes fusion. This review will discuss cutting-edge evidence that the FoxO-autophagy pathway plays an essential regulator in the pathogenesis of osteoarthritis.

Arthroscopic repair of the medium-size rotator cuff tear with the novel technique of the point union bridge: a minimum 2-year follow-up cohort study.

BACKGROUND: Achieving secure fixation and preventing retear have been recognized as fundamental in arthroscopic repair of rotator cuff tears. Moreover, reducing internal implantation can lower medical expenses and minimize the operation time, which is essential for the surgical safety and postoperative rehabilitation of the patients. We have recently proposed the point union bridge (PUB) suture configuration as a novel method for not only providing equivalent fixation but also decreasing the operation time and medical expenses. However, no comparative clinical studies have been performed. METHODS: From March 2014 to September 2016, a total of 88 patients with diagnoses of medium-size rotator cuff tears underwent arthroscopic repair with a randomly assigned technique-either the PUB technique (n = 42) or the double-row suture bridge (DRSB) technique (n = 46). All patients underwent a minimal 2-year follow-up. We used the Constant-Murley score (CMS), American Shoulder and Elbow Surgeons (ASES) score, active and passive range of motion, and visual pain-simulation score (visual analog scale [VAS] score) to assess the functional outcomes. In addition, we recorded the arthroscopic operation time, medical costs, and postoperative complications. All patients received magnetic resonance imaging at the 6-month and 2-year postoperative evaluations to assess structural integrity and tendon healing. RESULTS: At the 2-year follow-up, all scoring parameters evaluated (CMS, ASES score, and VAS score), as well as active and passive range of motion, improved significantly in both groups as compared with preoperative assessments. The PUB technique significantly decreased the operation time (55.9 ± 14.1 minutes vs. 72.2 ± 14.2 minutes for PUB vs. DRSB, P < .001) and medical expenses ($2608.0 ± $391.1 vs. $4056.9 ± $350.9 for PUB vs. DRSB, P < .001). However, no significant differences between the 2 techniques were found in any functional assessments of the shoulder (CMS, ASES score, and VAS score), repair integrity, or the retear rate at the 2-year follow-up. CONCLUSION: Arthroscopic repair of the medium-size rotator cuff tear with either the PUB or DRSB technique could yield both satisfactory improvements in the shoulder function of patients and equivalent tendon integrity. With less consumption of internal implants, the PUB technique significantly reduced the operation time and decreased medical expenses.

High concentration magnesium inhibits extracellular matrix calcification and protects articular cartilage via Erk/autophagy pathway.

The significant cytopathological changes of osteoarthritis are chondrocyte hypertrophy, proteoglycan loss, extracellular matrix (ECM) calcification, and terminally, the replacement of cartilage by bone. Meanwhile, magnesium ion (Mg2+ ), as the second most abundant divalent cation in the human body, has been proved to inhibit the ECM calcification of hBMSCs (human bone marrow stromal cells), hVSMCs (Human vascular smooth muscle cells), and TDSCs (tendon-derived stem cells) in vitro studies. The ATDC5 cell line, which holds chondrocyte characteristics, was used in this study as an in vitro subject. We found that Mg2+ can efficiently suppress the ECM calcification and downregulate both hypertrophy and matrix metalloproteinase-related genes. Meanwhile, Mg2+ inhibits the formation of autophagy by inhibiting Erk phosphorylation signaling and lowers the expression of LC3, and eventually effectively reduces the formation of ECM calcification in vitro. In this study, we also used destabilization of the medial meniscus (DMM)-induced osteoarthritis (OA) animal model to further confirm the protective effect of Mg2+ on articular cartilage. Compared with the control group (saline-injected), continuous intra-articular magnesium chloride (MgCl2 ) injection can significantly alleviate the severity of cartilage calcification in OA animal model. Immunofluorescence staining also revealed that saline-injected DMM group had a higher positive rate of LC3 expression in cartilage chondrocytes, compared with MgCl2 -injected DMM group. In general, Mg2+ can significantly downregulate the hypertrophic gene Runx2, MMP13, and Col10α1, upregulate the chondrogenic genes Sox9 and Col1α1, inhibit the Erk phosphorylation signaling, reduce the expression of autophagy protein LC3, and effectively inhibit the ECM calcification of ATDC5. In vivo study also proved that intra-articular injection of Mg2+ protected knee cartilage by inhibiting the autophagy formation.

High magnesium prevents matrix vesicle-mediated mineralization in human bone marrow-derived mesenchymal stem cells via mitochondrial pathway and autophagy.

Magnesium, as a physiological calcium antagonist, plays a vital role in the bone metabolism and the balance between magnesium and calcium is crucial in bone physiology. We recently demonstrated that matrix mineralization in human bone marrow-derived mesenchymal stem cells (hBMSCs) can be suppressed by high Mg2+ . However, a complete understanding of the mechanisms involved still remains to be elucidated. As mitochondrial calcium phosphate granules depletion manifests concurrently with the appearance of matrix vesicles (MVs) and autophagy are associated with matrix mineralization, we studied the effect of high extracellular Mg2+ on these pathways. Our results first demonstrated that high Mg2+ has a significant inhibitory effect on the generalization of extracellular mineral aggregates and the expression of collagen 1 along which the mineral crystals grow. Transmission electron microscope results showed that less amount of MVs were observed inside hBMSCs treated with high Mg2+ and high Mg2+ inhibited the release of MVs. In addition, high Mg2+ significantly suppressed mitochondrial Ca2+ accumulation. Autophagy is promoted as a response to osteogenesis of hBMSCs. High Mg2+ inhibited the level of autophagy upon osteogenesis and autophagy inhibitor 3-MA significantly suppressed mineralization. Exogenous ATP can reverse the inhibitory effect of high Mg2+ by increasing the level of autophagy. Taken together, our results indicate that high Mg2+ may modulate MVs-mediated mineralization via suppressing mitochondrial Ca2+ intensity and regulates autophagy of hBMSCs upon osteogenesis, resulting in decreased extracellular mineralized matrix deposition. Our results contribute to the understanding of the role of magnesium homeostasis in osteoporosis and the design of magnesium alloys.

Magnesium inhibits the calcification of the extracellular matrix in tendon-derived stem cells via the ATP-P2R and mitochondrial pathways.

Tendon calcification has been widely regarded by researchers to result from the osteogenic differentiation of Tendon-Derived Stem Cells (TDSCs) and ectopic mineralization caused by the calcification of cellular matrix. Recent studies have revealed a correlation between the Mg(2+)/Ca(2+) balance and the degeneration or calcification of tendon tissues. Furthermore, the ATP-P2X/P2Y receptor pathway has been shown to play a decisive role in the process of calcification, with calcium exportation from mitochondria and calcium oscillations potentially representing the cohesive signal produced by this pathway. Our previous study demonstrated that matrix calcification is inhibited by magnesium. In this study, we examined the effects of extracellular Mg(2+) on the deposition of calcium phosphate matrix and cellular pathways in TDSCs. The suppression of the export of calcium from mitochondria has also been detected. We found that a high concentration of extracellular Mg(2+) ([Mg(2+)]e) inhibited the mineralization of the extracellular matrix in TDSCs and that 100 µM ATP reversed this inhibitory effect in vitro. In addition, the spontaneous release of ATP was inhibited by high [Mg(2+)]e levels. A high [Mg(2+)]e suppressed the expression of P2X4, P2X5 and P2X7 and activated the expression of P2Y1, P2Y2, P2Y4 and P2Y14. The interaction between Mg(2+) and Ca(2+) is therefore contradictory, Mg(2+) inhibits mitochondrial calcium concentrations, meanwhile it reverses the opening of mPTP that is induced by Ca(2+). JC-1 staining verified the protective effect of Mg(2+) on mitochondrial membrane potential and the decrease induced by Ca(2+). Taken together, these results indicate that high [Mg(2+)]e interferes with the expression of P2 receptors, resulting in decreased extracellular mineralization. The balance between Mg(2+) and Ca(2+) influences mitochondrial calcium exportation and provides another explanation for the mechanism underlying matrix calcification in TDSCs.

The impact of patellofemoral arthritis on unicompartmental knee arthroplasty.

Unicompartmental knee arthroplasty (UKA) is an efficient surgical treatment for osteoarthritis or avascular osteonecrosis by resurfacing the medial or lateral compartment of the tibiofemoral joint. If compared to total knee arthroplasty (TKA), UKA can reach the same long-term curative effect, but superiority in less invasive soft tissue dissection, preservation of bone stock, minimal blood loss, faster post-operative rehabilitation and less complications. For the last 15 years, the Oxford Knee phase 3 has been implanted through a minimally invasive approach, and multicenter studies using this approach have reported high survival rates at long-term follow-up. Up to now, UKA has accounted for a significant portion of the patients who need knee replacement. However, there remain some controversies on UKA indications, such as the debate regarding associated patellofemoral arthritis as a contraindication for UKA. As clear indications for UKA are usually rare, surgeon's experience seems to be the key factor for a successful selection of patients. Better understanding of indications may add to improved outcome of UKA. This narrative review aims to summarize the current pros and cons to eliminate patellofemoral arthritis (PFA) as a contraindication for UKA.

Innovations in 3D printed individualized bone prosthesis materials: revolutionizing orthopedic surgery: a review.

The advent of personalized bone prosthesis materials and their integration into orthopedic surgery has made a profound impact, primarily as a result of the incorporation of three-dimensional (3D) printing technology. By leveraging digital models and additive manufacturing techniques, 3D printing enables the creation of customized, high-precision bone implants tailored to address complex anatomical variabilities and challenging bone defects. In this review, we highlight the significant progress in utilizing 3D printed prostheses across a wide range of orthopedic procedures, including pelvis, hip, knee, foot, ankle, spine surgeries, and bone tumor resections. The integration of 3D printing in preoperative planning, surgical navigation, and postoperative rehabilitation not only enhances treatment outcomes but also reduces surgical risks, accelerates recovery, and optimizes cost-effectiveness. Emphasizing the potential for personalized care and improved patient outcomes, this review underscores the pivotal role of 3D printed bone prosthesis materials in advancing orthopedic practice towards precision, efficiency, and patient-centric solutions. The evolving landscape of 3D printing in orthopedic surgery holds promise for revolutionizing treatment approaches, enhancing surgical outcomes, and ultimately improving the quality of care for orthopedic patients.

Carboxymethyl cellulose-based hydrogel with high-density crack microstructures inspired from the multi-tentacles of octopus for ultrasensitive flexible sensing microsystem.

Constructing high-density contact-separation sites on conductive materials highly determines the sensitivity of flexible resistance-type sensors relying on the crack microstructures. Herein, inspired from the multiple-tentacle structures on octopus, we demonstrated a sort of novel carbonized ZIF-8@loofah (CZL) as conductive material to develop ultrasensitivity flexible sensor, in which the carbonized ZIF-8 nanoparticles (~100 nm) served as tentacles. Originating from the formation of high-density contact-separation sites, the fabricated CZL-based strain sensor delivered ultrahigh sensitivity of GFmax = 15,901, short response time of 22 ms and excellent durability over 10,000 cycles. These features enable the sensor with efficient monitoring capacity for complex human activities, such as pulse rate and phonation. Moreover, when CZL was assembled into triboelectric nanogenerator (TENG), CZL-based TENG can effectively convert the irregular biomechanical energy into electric energy, providing sustainable power supply for the continuous operation of the sensing micro-system. Our findings established a novel platform to develop high-performance self-powered sensing systems of physiological parameter of human inspired from the nature.

RNA binding proteins in extracellular vesicles and their potential value for cancer diagnosis and treatment (Review).

Extracellular vesicles (EVs) are spherical bilayer membrane vesicles released by cells into extracellular spaces and body fluids, including plasma and synovial fluid. EV cargo comprises various biomolecules, such as proteins, DNA, mRNAs, non­coding RNAs, lipids and metabolites. By delivering these bioactive molecules to recipient cells, EVs mediate intercellular communications and play a critical role in maintaining cellular homeostasis and promoting pathological progression. Of note, cells can selectively sort these bioactive molecules (particularly RNAs) into EVs for secretion, as well as regulate cell­cell communications. RNA­binding proteins (RBPs) are a large class of proteins capable of binding to RNA molecules and function in regulating RNA metabolism. There is increasing evidence to indicate that RBPs can be delivered to receipt cells to influence their cell biology and play a significant role in the sorting of coding and non­coding RNAs in EVs. The present review summarized the current knowledge on EV­associated RBPs, their functions in tumorigenesis and RBP­related exosome engineering. It is hoped that the present review may provide novel insight into RBPs and targeted cancer treatment.

High-performance carboxymethyl cellulose-based composite film tailored by versatile zeolitic imidazolate framework.

Robust biopolymer-based composite film with multifunctional performances significantly contributes to the packaging field. Herein, we proposed a sort of carboxymethyl cellulose (CMC) based composite film via incorporating versatile zeolitic imidazolate framework (ZIF) materials. Compared to pristine CMC film, the OTR, WVTR, and tensile strength of CMC/ZIF composite film with 1 wt ‰ Zn/Co-ZIF were improved from 64.89 cm3*µm/(m2*d*kPa), 1579.21 g/(m2*24h) and 16.9 MPa to 20.79 cm3*µm/(m2*d*kPa), 1209.58 g/(m2*24h) and 70.1 MPa, respectively. Notably, owing to the reduced band gap and intrinsic chemical and thermal stability of Zn/Co-ZIF, the fabricated Zn/Co-ZIF/CMC composite film presented well UV protection capability within the whole UV region and excellent UV-blocking durability after being exposed to UV-light at 365 nm for 12 h. In practice, the photocatalytic degradation of RhB solutions under UV light could be effectively suppressed when using Zn/Co-ZIF/CMC film as UV protection layer. Our findings proposed the potential application of these versatile ZIF materials as functional nanofiller within biopolymer substances for UV protection and transparent packaging area.

Xanthohumol alleviates palmitate-induced inflammation and prevents osteoarthritis progression by attenuating mitochondria dysfunction/NLRP3 inflammasome axis.

Osteoarthritis (OA) is a prevalent chronic degenerative joint disease worldwide. Obesity has been linked to OA, and increased free fatty acid levels (e.g., palmitate) contribute to inflammatory responses and cartilage degradation. Xanthohumol (Xn), a bioactive prenylated chalcone, was shown to exhibit antioxidative, anti-inflammatory, and anti-obesity capacities in multiple diseases. However, a clear description of the preventive effects of Xn on obesity-associated OA is unavailable. This study aimed to assess the chondroprotective function of Xn on obesity-related OA. The in vitro levels of inflammatory and ECM matrix markers in human chondrocytes were assessed after the chondrocytes were treated with PA and Xn. Additionally, in vivo cartilage degeneration was assessed following oral administration of HFD and Xn. This study found that Xn treatment completely reduces the inflammation and extracellular matrix degradation caused by PA. The proposed mechanism involves AMPK signaling pathway activation by Xn, which increases mitochondrial biogenesis, attenuates mitochondrial dysfunction, and inhibits NLRP3 inflammasome and the NF-κB signaling pathway induced by PA. In summary, this study highlights that Xn could decrease inflammation reactions and the degradation of the cartilage matrix induced by PA by inhibiting the NLRP3 inflammasome and attenuating mitochondria dysfunction in human chondrocytes.

Denosumab versus zoledronic acid in cases of surgically unsalvageable giant cell tumor of bone: A randomized clinical trial.

Background: Giant-cell tumor of bone (GCTB) is a relatively benign, but locally aggressive osteoclastogenic stromal tumour of the bone. Although denosumab has been approved as an monoclonal antibody against RANK ligand for the treatment of GCTB, few clinical trials of the benefit in tumor response have been conducted to prove the efficiency in Chinese population. Objectives: In this multicentric, random controlled, clinical trial, 160 patients were enrolled to compare the therapeutic efficacy and safety of denosumab and zoledronic acid treatment in patients with surgically unsalvageable GCTB. Methods: Between 2nd Jan 2015 and 1st Jan 2018, 160 adults (aged ≥ 18 years) with ①surgically unsalvageable GCTB, ②surgically salvageable GCTB with planned surgery expected to result in severe morbidity were included in this randomized clinical trial. Patients received either subcutaneous denosumab (DB group; 120 mg once every 4 weeks with loading doses of 120 mg subcutaneously admininstered on days 8 and 15; n = 80) or intravenous zoledronic acid (ZA group; 4 mg once every 4 weeks; n = 80) for six cycles. Disease status, clinical benefits, treatment-emergent adverse effects, overall survival, and cost of treatment were evaluated during the follow-up period. Statistical significance was determined using 95% confidence intervals. Results: Denosumab and zoledronic acid had similar tumor responses (p = 0.118) and clinical benefits (p = 0.574). Disease progression was observed in fewer patients in the DB group (12.5%) than ZA group (15.0%). Denosumab caused fatigue (p = 0.001) and back pain (p < 0.0001), while zoledronic acid caused hypocalcemia (p < 0.0001), flu-like symptoms (p = 0.059) and hypotension (p = 0.059). Denosumab treatment was markedly more expensive than zoledronic acid treatment (p < 0.0001). The cost to manage treatment-emergent adverse effects was the same for the ZA group and the DB group (p = 0.425). The accumulate recurrence-free survival rate at 4-year follow-up is higher in DB group (p = 0.035). Conclusions: Denosumab is a safe but costly alternative to zoledronic acid for treatment of surgically unsalvageable GCTB.

Functions and therapeutic potentials of exosomes in osteosarcoma.

Osteosarcoma is a primary malignant tumor of the skeleton with the morbidity of 2.5 in 1 million. The regularly on-set is in the epiphysis of the extremities with a high possibility of early metastasis, rapid progression, and poor prognosis. The survival rate of patients with metastatic or recurrent osteosarcoma remains low, and novel diagnostic and therapeutic methods are urgently needed. Exosomes are extracellular vesicles 30-150 nm in diameter secreted by various cells that are widely present in various body fluids. Exosomes are abundant in biologically active components such as proteins, nucleic acids, and lipids. Exosomes participate in numerous physiological and pathological processes via intercellular substance exchange and signaling. This review presents the novel findings of exosomes in osteosarcoma in diagnosis, prognosis, and therapeutic aspects.

RNA binding proteins in osteoarthritis.

Osteoarthritis (OA) is a common chronic degenerative joint disease worldwide. The pathological features of OA are the erosion of articular cartilage, subchondral bone sclerosis, synovitis, and metabolic disorder. Its progression is characterized by aberrant expression of genes involved in inflammation, proliferation, and metabolism of chondrocytes. Effective therapeutic strategies are limited, as mechanisms underlying OA pathophysiology remain unclear. Significant research efforts are ongoing to elucidate the complex molecular mechanisms underlying OA focused on gene transcription. However, posttranscriptional alterations also play significant function in inflammation and metabolic changes related diseases. RNA binding proteins (RBPs) have been recognized as important regulators in posttranscriptional regulation. RBPs regulate RNA subcellular localization, stability, and translational efficiency by binding to their target mRNAs, thereby controlling their protein expression. However, their role in OA is less clear. Identifying RBPs in OA is of great importance to better understand OA pathophysiology and to figure out potential targets for OA treatment. Hence, in this manuscript, we summarize the recent knowledge on the role of dysregulated RBPs in OA and hope it will provide new insight for OA study and targeted treatment.

Caffeic acid phenethyl ester attenuates osteoarthritis progression by activating NRF2/HO­1 and inhibiting the NF­κB signaling pathway.

Osteoarthritis (OA) is the most common degenerative disease affecting the joints, and inflammation appears to play a critical role in the initiation and progression of OA. Caffeic acid phenethyl ester (CAPE), a natural flavonoid compound, has anti­inflammatory and antioxidant functions. However, its anti­inflammatory effects on OA and the underlying mechanisms of action of CAPE in the treatment of OA remain elusive. Therefore, the present study investigated the anti­inflammatory effects of CAPE on IL­1ß­stimulated chondrocytes in vitro and surgically induced rat models of OA in vivo. In vitro, CAPE reduced the expression of inducible nitric oxide synthase and cyclooxygenase­2 in IL­1ß­stimulated chondrocytes, as well as the extracellular secretion of nitric oxide and prostaglandin E2 in the cell culture supernatants. In addition, CAPE attenuated the degradation of extracellular matrix by increasing the expression of aggrecan and collagen II, and decreasing the expression of MMP3, MMP13 and a disintegrin and metalloproteinase with thrombospondin motif­5. Furthermore, CAPE attenuated NF­κB signaling and activated the nuclear factor erythroid 2­related factor 2/heme oxygenase­1 signaling pathway in IL­1ß­stimulated chondrocytes. In vivo, CAPE protected cartilage from destruction and delayed the progression of OA in rats. Taken together, the findings of the present study indicated that CAPE may be a potential therapeutic agent for the prevention or treatment of OA.

Arthroscopic acetabular labrum reconstruction with capsular autograft: clinical outcome and preliminary results.

To introduce a novel technique to reconstruct the acetabular labrum using capsular autograft, and to evaluate the preliminary clinical outcome, a retrospective review of a prospectively collected registry was undertaken that identified 21 patients (21 hips) who underwent arthroscopic reconstruction of the labrum by capsular autograft from January 2016 to January 2018. Modified Harris Hip Score (mHHS), Hip Outcome Score (HOS), and Hip Outcome Score-Activities of Daily Living (HOS-ADL) were recorded preoperatively and postoperatively. Clinical outcome was analyzed to evaluate the effectiveness of this technique. Twenty-one patients, with an average follow-up time of 25.4 ± 1.6 months, were included in this study: 7 patients were diagnosed with hypoplastic labrum (width <5 mm), 9 patients with complex tear of labrum, and 5 patients with degenerative labrum. The mHHS (61.3 ± 5.5 vs. 87.5 ± 4.2, P<0.001), HOS (52.5 ± 5.1 vs. 87.3 ± 3.8, P<0.001) and HOS-ADL (48.5 ± 5.8% vs. 75.2 ± 3.5%, P<0.001) between preoperative and the 6-month follow-up were significantly different. Gender exerts no influence on the outcome of mHHS, HOS and HOS-ADL. Therefore, local capsular autograft is readily available during arthroscopy with no donor-site morbidity. The reconstruction of the hip labrum may be valuable for patients with hypoplastic or dysplastic labrum, complex tear of labrum and severe degeneration. With appropriate patient selection, this technique is promising in preliminary clinical outcome.

[Research progress about influence of patellofemoral osteoarthritis on effectiveness of unicompartmental knee arthroplasty].

Objective: To summarize the current research progress about influence of patellofemoral osteoarthritis on clinical outcome of unicompartmental knee arthroplasty (UKA). Methods: The recent related literature was extensively reviewed and summarized, including pros and cons to regard the patellofemoral osteoarthritis as the contraindication. Results: Previous studies regarded patellofemoral osteoarthritis as the contraindication of UKA. Most of current researches show that the damage to the articular cartilage of the patellofemoral joint to the extent of full-thickness cartilage loss has no influence on outcome of UKA. There is no correlation between preoperative anterior knee pain or medial patellofemoral joint degeneration and the clinical outcome. However, lateral subluxation of the patella has an adverse impact on postoperative curative effect. Degeneration of the lateral patellofemoral joint may be a risk factor of the outcome. Conclusion: Patellofemoral osteoarthritis should not be the absolute contraindication of UKA. The effect of degeneration of the lateral patellofemoral joint is not clear at present, and still needs further studies in the future.

Comparative effectiveness of extracorporeal shock wave, ultrasound, low-level laser therapy, noninvasive interactive neurostimulation, and pulsed radiofrequency treatment for treating plantar fasciitis: A systematic review and network meta-analysis.

BACKGROUND: Plantar fasciitis is one of the most common causes of adult heel pain. The aim of this study is to comprehensively compare the effectiveness of various therapies for plantar fasciitis using network meta-analysis. METHODS: Studies were comprehensively searched on Embase, MEDLINE via PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), and the Physiotherapy Evidence Database (PEDro) up to December 4, 2017. Randomized controlled trials that used extracorporeal shock wave therapy, ultrasound, ultrasound-guided pulsed radiofrequency treatment (UG-PRF), intracorporeal pneumatic shock therapy (IPST), low-level laser therapy (LLLT), and noninvasive interactive neurostimulation (NIN) for the treatment of plantar fasciitis were included. The primary outcome is change in pain relief. Risk of bias was assessed using the Cochrane risk of bias tool. Quality assessment was performed using the GRADE system. RESULTS: Nineteen trials with 1676 patients with plantar fasciitis plantar fasciitis were included. In the pair-wise meta-analysis, radial extracorporeal shock wave therapy (RSW), LLLT, and IPST showed a significant pooled reduction in the visual analogue scale (VAS) compared with placebo at 0 to 6 weeks [mean difference (MD) = 6.60, 95% confidence interval (CI): (6.04, -7.16); MD = 2.34, 95% CI: (1.60, 3.08); MD = 2.24, 95% CI: (1.44, 3.04), respectively]. Compared with placebo, UG-PRF [MD = 2.31, 95% CI: (1.26, 3.36)] and high-intensity focused extracorporeal shock wave (H-FSW) [MD = 0.82, 95% CI: (0.20, 1.45)] showed superior pain-relieving effects at 2 to 4 months; UG-PRF [MD = 1.11, 95% CI: (0.07, 2.15)] and IPST [MD = 4.92, 95% CI: (4.11, 5.73)] showed superior effects at 6 to 12 months. In the network meta-analysis, only RSW induced significant pain reduction compared with placebo at 0 to 6 weeks [MD = 3.67, 95% CI: (0.31, 6.9)]. No significant differences were found for the 2 to 4-month and 6 to 12-month periods because of the wide 95% CIs. CONCLUSIONS: We recommend treating plantar fasciitis with RSW. The commonly used ultrasound and focused extracorporeal shock wave (FSW) therapies can be considered as alternative treatment candidates. IPST, NIN, and LLLT may potentially be better alternatives, although their superiority should be confirmed by additional comprehensive evidence.PROSPERO registration number: PROSPERO (CRD42015017353).

Unraveling the role of Mg(++) in osteoarthritis.

Mg(++) is widely involved in human physiological processes that may play key roles in the generation and progression of diseases. Osteoarthritis (OA) is a complex joint disorder characterized by articular cartilage degradation, abnormal mineralization and inflammation. Magnesium deficiency is considered to be a major risk factor for OA development and progression. Magnesium deficiency is active in several pathways that have been implicated in OA, including increased inflammatory mediators, cartilage damage, defective chondrocyte biosynthesis, aberrant calcification and a weakened effect of analgesics. Abundant in vitro and in vivo evidence in animal models now suggests that the nutritional supplementation or local infiltration of Mg(++) represent effective therapies for OA. The goal of this review is to summarize the current understanding of the role of Mg(++) in OA with particular emphasis on the related molecular mechanisms involved in OA progression.